Anxiety disorders: Psychopharmacologic treatment update

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Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.

Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.

AGrigorjeva/Thinkstock
Boy with head in hands, children with rucksacks sitting on the stairs near school

With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
 

SSRIs and SNRIs

A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4

Benzodiazepines

Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.

Guanfacine

In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.

Atomoxetine

A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.

Buspirone

This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7

Antipsychotics

Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.

 

 

Summary

Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.

Dr. David C. Rettew
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Follow him on Twitter @PediPsych.

Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.

 

References

1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.

2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.

3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.

4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.

5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..

6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.

7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.




 

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Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.

Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.

AGrigorjeva/Thinkstock
Boy with head in hands, children with rucksacks sitting on the stairs near school

With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
 

SSRIs and SNRIs

A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4

Benzodiazepines

Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.

Guanfacine

In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.

Atomoxetine

A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.

Buspirone

This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7

Antipsychotics

Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.

 

 

Summary

Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.

Dr. David C. Rettew
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Follow him on Twitter @PediPsych.

Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.

 

References

1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.

2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.

3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.

4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.

5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..

6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.

7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.




 

Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.

Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.

AGrigorjeva/Thinkstock
Boy with head in hands, children with rucksacks sitting on the stairs near school

With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
 

SSRIs and SNRIs

A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4

Benzodiazepines

Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.

Guanfacine

In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.

Atomoxetine

A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.

Buspirone

This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7

Antipsychotics

Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.

 

 

Summary

Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.

Dr. David C. Rettew
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Follow him on Twitter @PediPsych.

Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.

 

References

1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.

2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.

3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.

4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.

5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..

6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.

7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.




 

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How to help children process, overcome horrific traumas

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Unfathomable. Unspeakable.

These are among the terms used to describe children’s extreme traumatic experiences such as severe abuse and neglect. It is often most shocking when these acts are perpetrated by the children’s parents – the very ones that children should be able to depend on for their protection and safety.

Many believe that, in addition to the cumulative and serious nature of repetitive interpersonal traumas themselves, this betrayal of trust will result in irreparable psychological damage. Fortunately, this does not have to be the case. Children are more resilient than we realize; with safety, support, and effective treatment, they can recover from even the most extreme traumas and live healthy, productive lives.

The first priority is for child-serving systems to remove children from severely abusive situations and allow them to live in safe, stable, supportive settings while minimizing traumatic separation from siblings or further disruptions in their living situation. Acute medical problems need to be stabilized, and a thorough mental health assessment should be conducted.

Evidence-based trauma-focused psychotherapy is the first-line treatment for addressing pediatric posttraumatic stress disorder (J Am Acad Child Adolesc Psychiatry. 2010 Apr;49[4]:414-30). Several treatments are currently available. A few examples are trauma-focused cognitive-behavioral therapy, or TF-CBT, for children aged 3-18 years; child-parent psychotherapy (CPP) for children aged 0-6 years; a group school-based model, cognitive behavioral interventions for trauma in schools (CBITS); and Trauma Affect Regulation: Guide for Education and Therapy for teens (TARGET).

Common elements of evidence-based trauma-focused treatments are: 1) nonperpetrating caregivers are included in therapy to enhance support and understanding of the child’s trauma responses, and to address trauma-related behavioral problems; 2) skills are provided to the youth and caregiver for coping with negative trauma-related thoughts, feelings, and behaviors; and 3) children are supported to directly talk about and make meaning of their trauma experiences.

Through trauma-focused treatment, children become able to cope with their traumatic experiences and memories – make sense out of them. These traumas are no longer “unfathomable or “unspeakable,” but rather, manageable memories of bad experiences that the children have had the courage to face and master.

Children can recover from even extreme trauma experiences when they receive effective trauma-focused treatment in the context of a supportive environment. More information about evidence-based treatments is available from the National Child Traumatic Stress Network at www.nctsn.org/resources/topics/treatments-that-work/promising-practices.
 

Dr. Judith A. Cohen
Dr. Cohen, a board-certified child psychiatrist, is medical director of the Center for Traumatic Stress in Children and Adolescents at Allegheny General Hospital in Pittsburgh. She is codeveloper of TF-CBT, described in Treating Trauma and Traumatic Grief in Children and Adolescents and Trauma-Focused CBT for Children and Adolescents: Treatment Applications (New York: Guilford Press, 2012). She receives grant funding from National Institute of Mental Health, the National Institute of Child Health and Human Development, and the Substance Abuse and Mental Health Services Administration. In addition, Dr. Cohen receives royalties from Guilford Press, Oxford Press, UpToDate, and other TF-CBT products. She does not receive industry funding.

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Unfathomable. Unspeakable.

These are among the terms used to describe children’s extreme traumatic experiences such as severe abuse and neglect. It is often most shocking when these acts are perpetrated by the children’s parents – the very ones that children should be able to depend on for their protection and safety.

Many believe that, in addition to the cumulative and serious nature of repetitive interpersonal traumas themselves, this betrayal of trust will result in irreparable psychological damage. Fortunately, this does not have to be the case. Children are more resilient than we realize; with safety, support, and effective treatment, they can recover from even the most extreme traumas and live healthy, productive lives.

The first priority is for child-serving systems to remove children from severely abusive situations and allow them to live in safe, stable, supportive settings while minimizing traumatic separation from siblings or further disruptions in their living situation. Acute medical problems need to be stabilized, and a thorough mental health assessment should be conducted.

Evidence-based trauma-focused psychotherapy is the first-line treatment for addressing pediatric posttraumatic stress disorder (J Am Acad Child Adolesc Psychiatry. 2010 Apr;49[4]:414-30). Several treatments are currently available. A few examples are trauma-focused cognitive-behavioral therapy, or TF-CBT, for children aged 3-18 years; child-parent psychotherapy (CPP) for children aged 0-6 years; a group school-based model, cognitive behavioral interventions for trauma in schools (CBITS); and Trauma Affect Regulation: Guide for Education and Therapy for teens (TARGET).

Common elements of evidence-based trauma-focused treatments are: 1) nonperpetrating caregivers are included in therapy to enhance support and understanding of the child’s trauma responses, and to address trauma-related behavioral problems; 2) skills are provided to the youth and caregiver for coping with negative trauma-related thoughts, feelings, and behaviors; and 3) children are supported to directly talk about and make meaning of their trauma experiences.

Through trauma-focused treatment, children become able to cope with their traumatic experiences and memories – make sense out of them. These traumas are no longer “unfathomable or “unspeakable,” but rather, manageable memories of bad experiences that the children have had the courage to face and master.

Children can recover from even extreme trauma experiences when they receive effective trauma-focused treatment in the context of a supportive environment. More information about evidence-based treatments is available from the National Child Traumatic Stress Network at www.nctsn.org/resources/topics/treatments-that-work/promising-practices.
 

Dr. Judith A. Cohen
Dr. Cohen, a board-certified child psychiatrist, is medical director of the Center for Traumatic Stress in Children and Adolescents at Allegheny General Hospital in Pittsburgh. She is codeveloper of TF-CBT, described in Treating Trauma and Traumatic Grief in Children and Adolescents and Trauma-Focused CBT for Children and Adolescents: Treatment Applications (New York: Guilford Press, 2012). She receives grant funding from National Institute of Mental Health, the National Institute of Child Health and Human Development, and the Substance Abuse and Mental Health Services Administration. In addition, Dr. Cohen receives royalties from Guilford Press, Oxford Press, UpToDate, and other TF-CBT products. She does not receive industry funding.

 

Unfathomable. Unspeakable.

These are among the terms used to describe children’s extreme traumatic experiences such as severe abuse and neglect. It is often most shocking when these acts are perpetrated by the children’s parents – the very ones that children should be able to depend on for their protection and safety.

Many believe that, in addition to the cumulative and serious nature of repetitive interpersonal traumas themselves, this betrayal of trust will result in irreparable psychological damage. Fortunately, this does not have to be the case. Children are more resilient than we realize; with safety, support, and effective treatment, they can recover from even the most extreme traumas and live healthy, productive lives.

The first priority is for child-serving systems to remove children from severely abusive situations and allow them to live in safe, stable, supportive settings while minimizing traumatic separation from siblings or further disruptions in their living situation. Acute medical problems need to be stabilized, and a thorough mental health assessment should be conducted.

Evidence-based trauma-focused psychotherapy is the first-line treatment for addressing pediatric posttraumatic stress disorder (J Am Acad Child Adolesc Psychiatry. 2010 Apr;49[4]:414-30). Several treatments are currently available. A few examples are trauma-focused cognitive-behavioral therapy, or TF-CBT, for children aged 3-18 years; child-parent psychotherapy (CPP) for children aged 0-6 years; a group school-based model, cognitive behavioral interventions for trauma in schools (CBITS); and Trauma Affect Regulation: Guide for Education and Therapy for teens (TARGET).

Common elements of evidence-based trauma-focused treatments are: 1) nonperpetrating caregivers are included in therapy to enhance support and understanding of the child’s trauma responses, and to address trauma-related behavioral problems; 2) skills are provided to the youth and caregiver for coping with negative trauma-related thoughts, feelings, and behaviors; and 3) children are supported to directly talk about and make meaning of their trauma experiences.

Through trauma-focused treatment, children become able to cope with their traumatic experiences and memories – make sense out of them. These traumas are no longer “unfathomable or “unspeakable,” but rather, manageable memories of bad experiences that the children have had the courage to face and master.

Children can recover from even extreme trauma experiences when they receive effective trauma-focused treatment in the context of a supportive environment. More information about evidence-based treatments is available from the National Child Traumatic Stress Network at www.nctsn.org/resources/topics/treatments-that-work/promising-practices.
 

Dr. Judith A. Cohen
Dr. Cohen, a board-certified child psychiatrist, is medical director of the Center for Traumatic Stress in Children and Adolescents at Allegheny General Hospital in Pittsburgh. She is codeveloper of TF-CBT, described in Treating Trauma and Traumatic Grief in Children and Adolescents and Trauma-Focused CBT for Children and Adolescents: Treatment Applications (New York: Guilford Press, 2012). She receives grant funding from National Institute of Mental Health, the National Institute of Child Health and Human Development, and the Substance Abuse and Mental Health Services Administration. In addition, Dr. Cohen receives royalties from Guilford Press, Oxford Press, UpToDate, and other TF-CBT products. She does not receive industry funding.

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Antibiotic choice for acute otitis media 2018

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It’s a new year and a new respiratory season so my thoughts turn to the most common infection in pediatrics where an antibiotic might appropriately be prescribed – acute otitis media (AOM). The guidelines of the American Academy of Pediatrics were finalized in 2012 and published in 2013 and based on data that the AAP subcommittee considered. A recommendation emerged for amoxicillin to remain the treatment of choice if an antibiotic was to be prescribed at all, leaving the observation option as a continued consideration under defined clinical circumstances. The oral alternative antibiotics recommended were amoxicillin/clavulanate and cefdinir (Pediatrics. 2013. doi: 10.1542/peds.2012-3488).

Since the AAP subcommittee deliberated, changes have occurred in AOM etiology and the frequency of antibiotic resistance among the common bacteria that cause the infection. Our group in Rochester (N.Y.) continues to be the only site in the United States conducting a prospective assessment of AOM; we hope our data are generalizable to the entire country, but that is not certain. In Rochester, we saw an overall drop in AOM incidence after introduction of Prevnar 7 of about 10%-15% overall and that corresponded reasonably well with the frequency of AOM caused by Streptococcus pneumoniae involving the seven serotypes in the PCV7 vaccine. We then had a rebound in AOM infections, largely caused by serotype 19A, such that the overall incidence of AOM returned back to levels nearly the same as before PCV7 by 2010. With the introduction of Prevnar 13, and the dramatic reduction of serotype 19A nasal colonization – a necessary precursor of AOM – the incidence of AOM overall fell again, and compared with the pre-PCV7 era, I estimate that we are seeing about 20%-25% less AOM today.

In late 2017, we published an article describing the epidemiology of AOM in the PCV era (Pediatrics. 2017 Aug. doi: 10.1542/peds.2017-0181), in which we described changes in otopathogen distribution over time from 1996 through 2016. It showed that by end of 2016, the predominant bacteria causing AOM were Haemophilus influenzae, accounting for 60% of all AOM (52% detected by culture from tympanocentesis and another 8% detected by polymerase chain reaction). Among the H. influenzae from middle ear fluid, beta-lactamase production occurred in 45%. Therefore, according to principles of infectious disease antibiotic efficacy predictions, use of amoxicillin in standard dose or high dose would not eradicate about half of the H. influenzae causing AOM. In the table included in this column, I show calculations of predicted outcomes from amoxicillin, amoxicillin/clavulanate, and cefdinir treatment based on the projected otopathogen mix and resistance frequencies of 2016. Added to the data on H. influenzae I have included results of S. pneumoniae high nonsusceptibility at 5% of strains and beta-lactamase production by Moraxella catarrhalis at 100% of strains.



Strictly based on in vitro susceptibility and the known otopathogen mix, the calculations show that amoxicillin could result in a maximum cure of 57%, amoxicillin/clavulanate of 99%, and cefdinir of 80% of treated children.

In vitro susceptibility has its limitations. Pharmacodynamic calculations would drop the predicted success of all three antibiotics because suboptimal absorption after oral dosing occurs with amoxicillin and amoxicillin/clavulanate more so than with cefdinir, thereby resulting in lower than predicted levels of antibiotic at the site of infection within the middle ear, whereas the achievable level of cefdinir with recommended dosing sometimes is below the desired in vitro cut point.

To balance that lowered predicted efficacy, each of the otopathogens has an associated “spontaneous cure rate” that is often quoted as being 20% for S. pneumoniae, 50% for H. influenzae, and 80% for M. catarrhalis. However, to be clear, those rates were derived largely from assessments about 5 days after antibiotic treatment was started with ineffective drugs or with placebos and do not account for the true spontaneous clinical cure rate of AOM if assessed in the first few days after onset (when pain and fever are at their peak) nor if assessed 14-30 days later when almost all children have been cured by their immune systems.

The calculations also do not account for overdiagnosis in clinical practice. Indeed, if the child does not have AOM, then the child will have a cure regardless of which antibiotic is selected. Rates of overdiagnosis of AOM have been assessed with various methods and are subject to limitations. But overall the data and most experts agree that overdiagnosis by pediatricians, family physicians, urgent care physicians, nurse practitioners, and physician assistants is in the range of 30%-50%.

Before the reader leaps to the conclusion that I am endorsing any particular antibiotic strictly based on predicted in vitro efficacy, I would state that many considerations must be given to whether to use an antibiotic for AOM, and which antibiotic to use, at what dose, and for what duration. This column is just pointing out a few key up-to-date facts for your consideration.
 

Dr. Michael E. Pichichero
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute at Rochester (N.Y.) General Hospital. He has no relevant financial disclosures. Email him at [email protected].

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It’s a new year and a new respiratory season so my thoughts turn to the most common infection in pediatrics where an antibiotic might appropriately be prescribed – acute otitis media (AOM). The guidelines of the American Academy of Pediatrics were finalized in 2012 and published in 2013 and based on data that the AAP subcommittee considered. A recommendation emerged for amoxicillin to remain the treatment of choice if an antibiotic was to be prescribed at all, leaving the observation option as a continued consideration under defined clinical circumstances. The oral alternative antibiotics recommended were amoxicillin/clavulanate and cefdinir (Pediatrics. 2013. doi: 10.1542/peds.2012-3488).

Since the AAP subcommittee deliberated, changes have occurred in AOM etiology and the frequency of antibiotic resistance among the common bacteria that cause the infection. Our group in Rochester (N.Y.) continues to be the only site in the United States conducting a prospective assessment of AOM; we hope our data are generalizable to the entire country, but that is not certain. In Rochester, we saw an overall drop in AOM incidence after introduction of Prevnar 7 of about 10%-15% overall and that corresponded reasonably well with the frequency of AOM caused by Streptococcus pneumoniae involving the seven serotypes in the PCV7 vaccine. We then had a rebound in AOM infections, largely caused by serotype 19A, such that the overall incidence of AOM returned back to levels nearly the same as before PCV7 by 2010. With the introduction of Prevnar 13, and the dramatic reduction of serotype 19A nasal colonization – a necessary precursor of AOM – the incidence of AOM overall fell again, and compared with the pre-PCV7 era, I estimate that we are seeing about 20%-25% less AOM today.

In late 2017, we published an article describing the epidemiology of AOM in the PCV era (Pediatrics. 2017 Aug. doi: 10.1542/peds.2017-0181), in which we described changes in otopathogen distribution over time from 1996 through 2016. It showed that by end of 2016, the predominant bacteria causing AOM were Haemophilus influenzae, accounting for 60% of all AOM (52% detected by culture from tympanocentesis and another 8% detected by polymerase chain reaction). Among the H. influenzae from middle ear fluid, beta-lactamase production occurred in 45%. Therefore, according to principles of infectious disease antibiotic efficacy predictions, use of amoxicillin in standard dose or high dose would not eradicate about half of the H. influenzae causing AOM. In the table included in this column, I show calculations of predicted outcomes from amoxicillin, amoxicillin/clavulanate, and cefdinir treatment based on the projected otopathogen mix and resistance frequencies of 2016. Added to the data on H. influenzae I have included results of S. pneumoniae high nonsusceptibility at 5% of strains and beta-lactamase production by Moraxella catarrhalis at 100% of strains.



Strictly based on in vitro susceptibility and the known otopathogen mix, the calculations show that amoxicillin could result in a maximum cure of 57%, amoxicillin/clavulanate of 99%, and cefdinir of 80% of treated children.

In vitro susceptibility has its limitations. Pharmacodynamic calculations would drop the predicted success of all three antibiotics because suboptimal absorption after oral dosing occurs with amoxicillin and amoxicillin/clavulanate more so than with cefdinir, thereby resulting in lower than predicted levels of antibiotic at the site of infection within the middle ear, whereas the achievable level of cefdinir with recommended dosing sometimes is below the desired in vitro cut point.

To balance that lowered predicted efficacy, each of the otopathogens has an associated “spontaneous cure rate” that is often quoted as being 20% for S. pneumoniae, 50% for H. influenzae, and 80% for M. catarrhalis. However, to be clear, those rates were derived largely from assessments about 5 days after antibiotic treatment was started with ineffective drugs or with placebos and do not account for the true spontaneous clinical cure rate of AOM if assessed in the first few days after onset (when pain and fever are at their peak) nor if assessed 14-30 days later when almost all children have been cured by their immune systems.

The calculations also do not account for overdiagnosis in clinical practice. Indeed, if the child does not have AOM, then the child will have a cure regardless of which antibiotic is selected. Rates of overdiagnosis of AOM have been assessed with various methods and are subject to limitations. But overall the data and most experts agree that overdiagnosis by pediatricians, family physicians, urgent care physicians, nurse practitioners, and physician assistants is in the range of 30%-50%.

Before the reader leaps to the conclusion that I am endorsing any particular antibiotic strictly based on predicted in vitro efficacy, I would state that many considerations must be given to whether to use an antibiotic for AOM, and which antibiotic to use, at what dose, and for what duration. This column is just pointing out a few key up-to-date facts for your consideration.
 

Dr. Michael E. Pichichero
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute at Rochester (N.Y.) General Hospital. He has no relevant financial disclosures. Email him at [email protected].

 

It’s a new year and a new respiratory season so my thoughts turn to the most common infection in pediatrics where an antibiotic might appropriately be prescribed – acute otitis media (AOM). The guidelines of the American Academy of Pediatrics were finalized in 2012 and published in 2013 and based on data that the AAP subcommittee considered. A recommendation emerged for amoxicillin to remain the treatment of choice if an antibiotic was to be prescribed at all, leaving the observation option as a continued consideration under defined clinical circumstances. The oral alternative antibiotics recommended were amoxicillin/clavulanate and cefdinir (Pediatrics. 2013. doi: 10.1542/peds.2012-3488).

Since the AAP subcommittee deliberated, changes have occurred in AOM etiology and the frequency of antibiotic resistance among the common bacteria that cause the infection. Our group in Rochester (N.Y.) continues to be the only site in the United States conducting a prospective assessment of AOM; we hope our data are generalizable to the entire country, but that is not certain. In Rochester, we saw an overall drop in AOM incidence after introduction of Prevnar 7 of about 10%-15% overall and that corresponded reasonably well with the frequency of AOM caused by Streptococcus pneumoniae involving the seven serotypes in the PCV7 vaccine. We then had a rebound in AOM infections, largely caused by serotype 19A, such that the overall incidence of AOM returned back to levels nearly the same as before PCV7 by 2010. With the introduction of Prevnar 13, and the dramatic reduction of serotype 19A nasal colonization – a necessary precursor of AOM – the incidence of AOM overall fell again, and compared with the pre-PCV7 era, I estimate that we are seeing about 20%-25% less AOM today.

In late 2017, we published an article describing the epidemiology of AOM in the PCV era (Pediatrics. 2017 Aug. doi: 10.1542/peds.2017-0181), in which we described changes in otopathogen distribution over time from 1996 through 2016. It showed that by end of 2016, the predominant bacteria causing AOM were Haemophilus influenzae, accounting for 60% of all AOM (52% detected by culture from tympanocentesis and another 8% detected by polymerase chain reaction). Among the H. influenzae from middle ear fluid, beta-lactamase production occurred in 45%. Therefore, according to principles of infectious disease antibiotic efficacy predictions, use of amoxicillin in standard dose or high dose would not eradicate about half of the H. influenzae causing AOM. In the table included in this column, I show calculations of predicted outcomes from amoxicillin, amoxicillin/clavulanate, and cefdinir treatment based on the projected otopathogen mix and resistance frequencies of 2016. Added to the data on H. influenzae I have included results of S. pneumoniae high nonsusceptibility at 5% of strains and beta-lactamase production by Moraxella catarrhalis at 100% of strains.



Strictly based on in vitro susceptibility and the known otopathogen mix, the calculations show that amoxicillin could result in a maximum cure of 57%, amoxicillin/clavulanate of 99%, and cefdinir of 80% of treated children.

In vitro susceptibility has its limitations. Pharmacodynamic calculations would drop the predicted success of all three antibiotics because suboptimal absorption after oral dosing occurs with amoxicillin and amoxicillin/clavulanate more so than with cefdinir, thereby resulting in lower than predicted levels of antibiotic at the site of infection within the middle ear, whereas the achievable level of cefdinir with recommended dosing sometimes is below the desired in vitro cut point.

To balance that lowered predicted efficacy, each of the otopathogens has an associated “spontaneous cure rate” that is often quoted as being 20% for S. pneumoniae, 50% for H. influenzae, and 80% for M. catarrhalis. However, to be clear, those rates were derived largely from assessments about 5 days after antibiotic treatment was started with ineffective drugs or with placebos and do not account for the true spontaneous clinical cure rate of AOM if assessed in the first few days after onset (when pain and fever are at their peak) nor if assessed 14-30 days later when almost all children have been cured by their immune systems.

The calculations also do not account for overdiagnosis in clinical practice. Indeed, if the child does not have AOM, then the child will have a cure regardless of which antibiotic is selected. Rates of overdiagnosis of AOM have been assessed with various methods and are subject to limitations. But overall the data and most experts agree that overdiagnosis by pediatricians, family physicians, urgent care physicians, nurse practitioners, and physician assistants is in the range of 30%-50%.

Before the reader leaps to the conclusion that I am endorsing any particular antibiotic strictly based on predicted in vitro efficacy, I would state that many considerations must be given to whether to use an antibiotic for AOM, and which antibiotic to use, at what dose, and for what duration. This column is just pointing out a few key up-to-date facts for your consideration.
 

Dr. Michael E. Pichichero
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute at Rochester (N.Y.) General Hospital. He has no relevant financial disclosures. Email him at [email protected].

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The times they are a-changin’ —Bob Dylan, 1964

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The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

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The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

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Hungry or what?

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“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock
I recently encountered an anecdote in one of the New York Times op-ed pieces by Perri Klass, MD, that got me thinking more broadly about the perception of hunger and its power to motivate (“Do parents make kids fat?” the New York Times, Jan. 8, 2018). Dr. Klass relates a story of an obesity specialist who herself had struggled with obesity. Despite her careful attention to everything she had learned about obesity management and breastfeeding, this woman was unprepared for giving birth to an infant who was “instantly a very dramatically hungry baby.”

The result was a year-long odyssey of pumping that included consultations with five different lactation consultants in the first frustrating month and a half. She eventually received some comforting advice from a pediatrician who reassured her that there was little research to guide her and to “just feed him; trust your instincts.”

While it is unfortunately true that there is very little good science we can fall back on when counseling women who are struggling with breastfeeding, I wonder about the wisdom of telling this mother to trust her instincts. I guess my hesitancy is based on 40 years of primary care pediatrics in which I could generally count on the instincts of young children, but their parents’ not so much. While maternal intuition is generally superior to the paternal version, I am hesitant to rely totally on either when facing a clinical dilemma such as defining hunger.

Is a fussy infant hungry because he seems to be comforted only by a bottle or breast? What about the fussy baby who is comforted by just a pacifier? What is the difference? There are several explanations, but it will require introducing the concept of nutrition deficiency.

Most babies who are satisfied with just a nipple, be it silicone or flesh, simply find sucking a comfort measure. A few, and I am sure you have seen some of them, are overly patient. They seem to be saying, “I need the calories, but you’re a good mom and I enjoy sucking. I can wait. Some day, you may make more milk or give me a bottle.” In the worst-case scenarios, their patience leaves these babies so nutritionally deficient that they can slip into apathy and die.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff
On the other end of the spectrum are infants who love to suck so much that they will ignore (or maybe lack) their own satiety center. They may be fussy for some other reason than hunger, most likely sleep deprivation, and will suck and swallow to comfort themselves even though they have met their nutritional needs. The surplus milk or formula is converted to unhealthy weight or is misdiagnosed as “reflux.” Could this phenomenon have a genetic basis? Has the mother in Dr. Klass’ scenario shared an inheritable problem with satiety with her infant?

There are no easy answers. As pediatricians, our job is to sort out those fussy “hungry” babies whose behavior means they are overtired from those who are nutritionally deficient, from those with a dysfunctional satiety center. Making the differentiation is difficult but much easier than helping parents ignore one of their instincts.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock
I recently encountered an anecdote in one of the New York Times op-ed pieces by Perri Klass, MD, that got me thinking more broadly about the perception of hunger and its power to motivate (“Do parents make kids fat?” the New York Times, Jan. 8, 2018). Dr. Klass relates a story of an obesity specialist who herself had struggled with obesity. Despite her careful attention to everything she had learned about obesity management and breastfeeding, this woman was unprepared for giving birth to an infant who was “instantly a very dramatically hungry baby.”

The result was a year-long odyssey of pumping that included consultations with five different lactation consultants in the first frustrating month and a half. She eventually received some comforting advice from a pediatrician who reassured her that there was little research to guide her and to “just feed him; trust your instincts.”

While it is unfortunately true that there is very little good science we can fall back on when counseling women who are struggling with breastfeeding, I wonder about the wisdom of telling this mother to trust her instincts. I guess my hesitancy is based on 40 years of primary care pediatrics in which I could generally count on the instincts of young children, but their parents’ not so much. While maternal intuition is generally superior to the paternal version, I am hesitant to rely totally on either when facing a clinical dilemma such as defining hunger.

Is a fussy infant hungry because he seems to be comforted only by a bottle or breast? What about the fussy baby who is comforted by just a pacifier? What is the difference? There are several explanations, but it will require introducing the concept of nutrition deficiency.

Most babies who are satisfied with just a nipple, be it silicone or flesh, simply find sucking a comfort measure. A few, and I am sure you have seen some of them, are overly patient. They seem to be saying, “I need the calories, but you’re a good mom and I enjoy sucking. I can wait. Some day, you may make more milk or give me a bottle.” In the worst-case scenarios, their patience leaves these babies so nutritionally deficient that they can slip into apathy and die.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff
On the other end of the spectrum are infants who love to suck so much that they will ignore (or maybe lack) their own satiety center. They may be fussy for some other reason than hunger, most likely sleep deprivation, and will suck and swallow to comfort themselves even though they have met their nutritional needs. The surplus milk or formula is converted to unhealthy weight or is misdiagnosed as “reflux.” Could this phenomenon have a genetic basis? Has the mother in Dr. Klass’ scenario shared an inheritable problem with satiety with her infant?

There are no easy answers. As pediatricians, our job is to sort out those fussy “hungry” babies whose behavior means they are overtired from those who are nutritionally deficient, from those with a dysfunctional satiety center. Making the differentiation is difficult but much easier than helping parents ignore one of their instincts.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

 

“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock
I recently encountered an anecdote in one of the New York Times op-ed pieces by Perri Klass, MD, that got me thinking more broadly about the perception of hunger and its power to motivate (“Do parents make kids fat?” the New York Times, Jan. 8, 2018). Dr. Klass relates a story of an obesity specialist who herself had struggled with obesity. Despite her careful attention to everything she had learned about obesity management and breastfeeding, this woman was unprepared for giving birth to an infant who was “instantly a very dramatically hungry baby.”

The result was a year-long odyssey of pumping that included consultations with five different lactation consultants in the first frustrating month and a half. She eventually received some comforting advice from a pediatrician who reassured her that there was little research to guide her and to “just feed him; trust your instincts.”

While it is unfortunately true that there is very little good science we can fall back on when counseling women who are struggling with breastfeeding, I wonder about the wisdom of telling this mother to trust her instincts. I guess my hesitancy is based on 40 years of primary care pediatrics in which I could generally count on the instincts of young children, but their parents’ not so much. While maternal intuition is generally superior to the paternal version, I am hesitant to rely totally on either when facing a clinical dilemma such as defining hunger.

Is a fussy infant hungry because he seems to be comforted only by a bottle or breast? What about the fussy baby who is comforted by just a pacifier? What is the difference? There are several explanations, but it will require introducing the concept of nutrition deficiency.

Most babies who are satisfied with just a nipple, be it silicone or flesh, simply find sucking a comfort measure. A few, and I am sure you have seen some of them, are overly patient. They seem to be saying, “I need the calories, but you’re a good mom and I enjoy sucking. I can wait. Some day, you may make more milk or give me a bottle.” In the worst-case scenarios, their patience leaves these babies so nutritionally deficient that they can slip into apathy and die.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff
On the other end of the spectrum are infants who love to suck so much that they will ignore (or maybe lack) their own satiety center. They may be fussy for some other reason than hunger, most likely sleep deprivation, and will suck and swallow to comfort themselves even though they have met their nutritional needs. The surplus milk or formula is converted to unhealthy weight or is misdiagnosed as “reflux.” Could this phenomenon have a genetic basis? Has the mother in Dr. Klass’ scenario shared an inheritable problem with satiety with her infant?

There are no easy answers. As pediatricians, our job is to sort out those fussy “hungry” babies whose behavior means they are overtired from those who are nutritionally deficient, from those with a dysfunctional satiety center. Making the differentiation is difficult but much easier than helping parents ignore one of their instincts.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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Beware the COPD exacerbation

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A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock
Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

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A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock
Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

 

A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock
Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

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Psychiatry Innovation Lab nurtures young businesses

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Mon, 04/16/2018 - 14:09

 

The future of mental health is in our own hands. As psychiatrists, we have a wealth of experience to fuel transformation in our field and improve care for our patients. What we lack is the space in which to share our ideas and turn them into tangible solutions like sustainable businesses, diagnostic devices, mobile apps, or prevention campaigns.

The Psychiatry Innovation Lab provides just that – it is an incubator nurturing early-stage ideas and ventures by investing in them through mentorship, education, funding, and collaboration opportunities within a community of mental health innovators.

Dr. Neha P. Chaudhary
Applications are open now for submissions. The American Psychiatry Association’s Workgroup on Psychiatry Innovation will review submissions and select the strongest based on several criteria, including value, viability, background, and impact. Finalists will receive expert mentorship from industry leaders in business, technology, medicine, investing, and government on how to improve the feasibility and effectiveness of the idea.

The lab’s main event is on Sunday, May 6, 2018, when leaders in psychiatry will gather alongside industry leaders at the Jacob Javits Convention Center in New York City during the American Psychiatric Association meeting for this fourth annual live event . At the event, finalists will pitch ideas “Shark Tank” style to a panel of expert judges. Finalists will work closely with industry leaders and audience members to fine-tune their ideas before pitching their revisions to the judges as well as to a live, voting audience, who together select the winners of cash awards and other prizes.

Dr. Reza Hosseini Ghomi
“It was exhilarating being up there,” said Swathi Krishna, MD, the Audience Choice Award winner of the 2016 Psychiatry Innovation Lab. “Within a short amount of time, we learned how to fine-tune our business plan, get our product to market, and find the right partners to take our company to the next level. Winning a cash prize helped gain the funding necessary to get the idea off the ground. The best part was feeling plugged into a growing community of innovators. It’s hard to find that in mental health.”

The Psychiatry Innovation Lab was founded in 2015 by Nina Vasan, MD, a Stanford (Calif.) University psychiatrist and author of Do Good Well: Your Guide to Leadership, Action, and Social Innovation (San Francisco: Jossey-Bass, 2013), with the purpose of catalyzing more entrepreneurship and innovation in mental health.

“The most meaningful part of the lab has been the impact that these ventures have had on the patients that we serve,” said Dr. Vasan, chair of the Psychiatry Innovation Lab and director of Brainstorm, the Stanford Laboratory for Brain Health Innovation and Entrepreneurship. “Year after year, psychiatrists come back and tell us that they are looking at their own patient care differently now. They’re looking for ways to be innovative, and we’re giving them the tools necessary to turn their clinical expertise into successful ventures.”

Applications are currently open online to pitch an idea in this year’s lab. Applications consist of brief answers to questions and a short YouTube video. The deadline for submissions is Friday, March 9, 2018. Anyone with innovative ideas, regardless of the stage, is invited to apply. The APA Workgroup on Psychiatry Innovation, which oversees the lab, welcomes ideas from people pitching for the first time to those working on their ideas full time. They noted that past finalists have come from all experience levels and a wide range of backgrounds, including students, CEOs, engineers, and psychiatrists.

Past winners and participants have come from a range of stages, from early start-ups to established companies, including NeuroLex Labs, which uses voice samples to detect behavioral health illness; Spring, which uses machine learning to determine the best depression treatment; Muse, which creates an EEG sensing headband to aid mindfulness practice; and Overdose Recovery Bracelet, which builds a wristband to deliver naloxone to people who have overdosed on opiates.

The diversity of ideas has been remarkable; ideas in the past have ranged from traditional for-profit businesses to nonprofits, educational and public health programs, and proposals for government reform. They address problems at all parts of the health care spectrum: prevention, diagnosis, treatment, systems, EMRs, and more.

“Many past ideas have revolved around technology such as artificial intelligence, social networking, or telemedicine,” Dr. Vasan said. “In addition to great ideas using technology, we encourage ideas in other domains like in education and human rights. Those ideas are especially important in solving the most pressing problems in our field today.”

In addition to those competing, anyone registered to attend the APA annual meeting can attend the event as an audience member or join a team and help as an innovation leader during the coaching portion of the program. Last year alone, more than 70% of the participants in the lab said that it was better than other educational events they have attended, 95% of participants found it useful, and participants made an average of six new contacts through the event.

“The Psychiatry Innovation Lab connected me to people who continue to inspire and educate me toward making a real impact with my own endeavors,” said Cody Rall, MD, founder of the YouTube channel Techforpsych and a 2016 semifinalist.

“The lab has grown dramatically. When we started we worked hard to find just one sponsor; last year we had 10 sponsors and over $25,000 in cash and prizes.” Dr. Vasan said. “We also had our first international finalist from Pakistan. The commitment to solving problems in mental health is taking off, and we want to ensure that psychiatrists are front and center in leading the change.”

For more information about joining the innovation lab or other ways to be involved, including sponsorship and judging, visit https://www.psychiatry.org/innovation or email Nina Taylor, APA deputy director of education, at [email protected].

This article was updated January 23, 2018.

 

 

Dr. Chaudhary is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; chief resident in child and adolescent psychiatry at Massachusetts General Hospital/McLean and clinical fellow at Harvard Medical School, both in Boston; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship. Dr. Ghomi is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; resident in psychiatry at the University of Washington, Seattle; chief medical officer at NeuroLex; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship.

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The future of mental health is in our own hands. As psychiatrists, we have a wealth of experience to fuel transformation in our field and improve care for our patients. What we lack is the space in which to share our ideas and turn them into tangible solutions like sustainable businesses, diagnostic devices, mobile apps, or prevention campaigns.

The Psychiatry Innovation Lab provides just that – it is an incubator nurturing early-stage ideas and ventures by investing in them through mentorship, education, funding, and collaboration opportunities within a community of mental health innovators.

Dr. Neha P. Chaudhary
Applications are open now for submissions. The American Psychiatry Association’s Workgroup on Psychiatry Innovation will review submissions and select the strongest based on several criteria, including value, viability, background, and impact. Finalists will receive expert mentorship from industry leaders in business, technology, medicine, investing, and government on how to improve the feasibility and effectiveness of the idea.

The lab’s main event is on Sunday, May 6, 2018, when leaders in psychiatry will gather alongside industry leaders at the Jacob Javits Convention Center in New York City during the American Psychiatric Association meeting for this fourth annual live event . At the event, finalists will pitch ideas “Shark Tank” style to a panel of expert judges. Finalists will work closely with industry leaders and audience members to fine-tune their ideas before pitching their revisions to the judges as well as to a live, voting audience, who together select the winners of cash awards and other prizes.

Dr. Reza Hosseini Ghomi
“It was exhilarating being up there,” said Swathi Krishna, MD, the Audience Choice Award winner of the 2016 Psychiatry Innovation Lab. “Within a short amount of time, we learned how to fine-tune our business plan, get our product to market, and find the right partners to take our company to the next level. Winning a cash prize helped gain the funding necessary to get the idea off the ground. The best part was feeling plugged into a growing community of innovators. It’s hard to find that in mental health.”

The Psychiatry Innovation Lab was founded in 2015 by Nina Vasan, MD, a Stanford (Calif.) University psychiatrist and author of Do Good Well: Your Guide to Leadership, Action, and Social Innovation (San Francisco: Jossey-Bass, 2013), with the purpose of catalyzing more entrepreneurship and innovation in mental health.

“The most meaningful part of the lab has been the impact that these ventures have had on the patients that we serve,” said Dr. Vasan, chair of the Psychiatry Innovation Lab and director of Brainstorm, the Stanford Laboratory for Brain Health Innovation and Entrepreneurship. “Year after year, psychiatrists come back and tell us that they are looking at their own patient care differently now. They’re looking for ways to be innovative, and we’re giving them the tools necessary to turn their clinical expertise into successful ventures.”

Applications are currently open online to pitch an idea in this year’s lab. Applications consist of brief answers to questions and a short YouTube video. The deadline for submissions is Friday, March 9, 2018. Anyone with innovative ideas, regardless of the stage, is invited to apply. The APA Workgroup on Psychiatry Innovation, which oversees the lab, welcomes ideas from people pitching for the first time to those working on their ideas full time. They noted that past finalists have come from all experience levels and a wide range of backgrounds, including students, CEOs, engineers, and psychiatrists.

Past winners and participants have come from a range of stages, from early start-ups to established companies, including NeuroLex Labs, which uses voice samples to detect behavioral health illness; Spring, which uses machine learning to determine the best depression treatment; Muse, which creates an EEG sensing headband to aid mindfulness practice; and Overdose Recovery Bracelet, which builds a wristband to deliver naloxone to people who have overdosed on opiates.

The diversity of ideas has been remarkable; ideas in the past have ranged from traditional for-profit businesses to nonprofits, educational and public health programs, and proposals for government reform. They address problems at all parts of the health care spectrum: prevention, diagnosis, treatment, systems, EMRs, and more.

“Many past ideas have revolved around technology such as artificial intelligence, social networking, or telemedicine,” Dr. Vasan said. “In addition to great ideas using technology, we encourage ideas in other domains like in education and human rights. Those ideas are especially important in solving the most pressing problems in our field today.”

In addition to those competing, anyone registered to attend the APA annual meeting can attend the event as an audience member or join a team and help as an innovation leader during the coaching portion of the program. Last year alone, more than 70% of the participants in the lab said that it was better than other educational events they have attended, 95% of participants found it useful, and participants made an average of six new contacts through the event.

“The Psychiatry Innovation Lab connected me to people who continue to inspire and educate me toward making a real impact with my own endeavors,” said Cody Rall, MD, founder of the YouTube channel Techforpsych and a 2016 semifinalist.

“The lab has grown dramatically. When we started we worked hard to find just one sponsor; last year we had 10 sponsors and over $25,000 in cash and prizes.” Dr. Vasan said. “We also had our first international finalist from Pakistan. The commitment to solving problems in mental health is taking off, and we want to ensure that psychiatrists are front and center in leading the change.”

For more information about joining the innovation lab or other ways to be involved, including sponsorship and judging, visit https://www.psychiatry.org/innovation or email Nina Taylor, APA deputy director of education, at [email protected].

This article was updated January 23, 2018.

 

 

Dr. Chaudhary is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; chief resident in child and adolescent psychiatry at Massachusetts General Hospital/McLean and clinical fellow at Harvard Medical School, both in Boston; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship. Dr. Ghomi is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; resident in psychiatry at the University of Washington, Seattle; chief medical officer at NeuroLex; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship.

 

The future of mental health is in our own hands. As psychiatrists, we have a wealth of experience to fuel transformation in our field and improve care for our patients. What we lack is the space in which to share our ideas and turn them into tangible solutions like sustainable businesses, diagnostic devices, mobile apps, or prevention campaigns.

The Psychiatry Innovation Lab provides just that – it is an incubator nurturing early-stage ideas and ventures by investing in them through mentorship, education, funding, and collaboration opportunities within a community of mental health innovators.

Dr. Neha P. Chaudhary
Applications are open now for submissions. The American Psychiatry Association’s Workgroup on Psychiatry Innovation will review submissions and select the strongest based on several criteria, including value, viability, background, and impact. Finalists will receive expert mentorship from industry leaders in business, technology, medicine, investing, and government on how to improve the feasibility and effectiveness of the idea.

The lab’s main event is on Sunday, May 6, 2018, when leaders in psychiatry will gather alongside industry leaders at the Jacob Javits Convention Center in New York City during the American Psychiatric Association meeting for this fourth annual live event . At the event, finalists will pitch ideas “Shark Tank” style to a panel of expert judges. Finalists will work closely with industry leaders and audience members to fine-tune their ideas before pitching their revisions to the judges as well as to a live, voting audience, who together select the winners of cash awards and other prizes.

Dr. Reza Hosseini Ghomi
“It was exhilarating being up there,” said Swathi Krishna, MD, the Audience Choice Award winner of the 2016 Psychiatry Innovation Lab. “Within a short amount of time, we learned how to fine-tune our business plan, get our product to market, and find the right partners to take our company to the next level. Winning a cash prize helped gain the funding necessary to get the idea off the ground. The best part was feeling plugged into a growing community of innovators. It’s hard to find that in mental health.”

The Psychiatry Innovation Lab was founded in 2015 by Nina Vasan, MD, a Stanford (Calif.) University psychiatrist and author of Do Good Well: Your Guide to Leadership, Action, and Social Innovation (San Francisco: Jossey-Bass, 2013), with the purpose of catalyzing more entrepreneurship and innovation in mental health.

“The most meaningful part of the lab has been the impact that these ventures have had on the patients that we serve,” said Dr. Vasan, chair of the Psychiatry Innovation Lab and director of Brainstorm, the Stanford Laboratory for Brain Health Innovation and Entrepreneurship. “Year after year, psychiatrists come back and tell us that they are looking at their own patient care differently now. They’re looking for ways to be innovative, and we’re giving them the tools necessary to turn their clinical expertise into successful ventures.”

Applications are currently open online to pitch an idea in this year’s lab. Applications consist of brief answers to questions and a short YouTube video. The deadline for submissions is Friday, March 9, 2018. Anyone with innovative ideas, regardless of the stage, is invited to apply. The APA Workgroup on Psychiatry Innovation, which oversees the lab, welcomes ideas from people pitching for the first time to those working on their ideas full time. They noted that past finalists have come from all experience levels and a wide range of backgrounds, including students, CEOs, engineers, and psychiatrists.

Past winners and participants have come from a range of stages, from early start-ups to established companies, including NeuroLex Labs, which uses voice samples to detect behavioral health illness; Spring, which uses machine learning to determine the best depression treatment; Muse, which creates an EEG sensing headband to aid mindfulness practice; and Overdose Recovery Bracelet, which builds a wristband to deliver naloxone to people who have overdosed on opiates.

The diversity of ideas has been remarkable; ideas in the past have ranged from traditional for-profit businesses to nonprofits, educational and public health programs, and proposals for government reform. They address problems at all parts of the health care spectrum: prevention, diagnosis, treatment, systems, EMRs, and more.

“Many past ideas have revolved around technology such as artificial intelligence, social networking, or telemedicine,” Dr. Vasan said. “In addition to great ideas using technology, we encourage ideas in other domains like in education and human rights. Those ideas are especially important in solving the most pressing problems in our field today.”

In addition to those competing, anyone registered to attend the APA annual meeting can attend the event as an audience member or join a team and help as an innovation leader during the coaching portion of the program. Last year alone, more than 70% of the participants in the lab said that it was better than other educational events they have attended, 95% of participants found it useful, and participants made an average of six new contacts through the event.

“The Psychiatry Innovation Lab connected me to people who continue to inspire and educate me toward making a real impact with my own endeavors,” said Cody Rall, MD, founder of the YouTube channel Techforpsych and a 2016 semifinalist.

“The lab has grown dramatically. When we started we worked hard to find just one sponsor; last year we had 10 sponsors and over $25,000 in cash and prizes.” Dr. Vasan said. “We also had our first international finalist from Pakistan. The commitment to solving problems in mental health is taking off, and we want to ensure that psychiatrists are front and center in leading the change.”

For more information about joining the innovation lab or other ways to be involved, including sponsorship and judging, visit https://www.psychiatry.org/innovation or email Nina Taylor, APA deputy director of education, at [email protected].

This article was updated January 23, 2018.

 

 

Dr. Chaudhary is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; chief resident in child and adolescent psychiatry at Massachusetts General Hospital/McLean and clinical fellow at Harvard Medical School, both in Boston; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship. Dr. Ghomi is a board member of the APA Psychiatry Innovation Lab and the APA Workgroup on Psychiatry Innovation; resident in psychiatry at the University of Washington, Seattle; chief medical officer at NeuroLex; and founding partner of Brainstorm: Stanford Laboratory for Brain Health Innovation and Entrepreneurship.

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Letter from the Editor

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Thu, 01/25/2018 - 14:52

 

GI & Hepatology News is one of the most widely read publications focused on the gastroenterology community and is the official newspaper of the AGA. The New Gastroenterologist is the AGA publication targeted to trainees and early career physicians. Recognizing the strength of both digital and print communication, the AGA has consolidated its communication media.

John I. Allen, MD, MBA, AGAF
Editor in Chief of GI & Hepatology News

When The New Gastroenterologist debuted almost 3 years ago, it provided a mechanism for the AGA to condense and disseminate information in a single publication for those of us in training or in the early stages of our careers. Since then, The New Gastroenterologist has become a valuable resource for the AGA community and beyond. It is with great excitement that in 2018, The New Gastroenterologist will switch to a primarily digital format. Content will be distributed in quarterly e-newsletters, which will allow for easier distribution via social media. This will allow for the creation of a website archive of past articles that can be easily queried and accessed. Additionally, The New Gastroenterologist will debut an “In Focus” series of concise updates on pertinent topics in our field. These In Focus articles will be published on a quarterly basis in GI & Hepatology News and will undoubtedly be practical and informative features that will be of interest to all AGA members, regardless of their career stage. The first In Focus article, which appears in this issue of GI & Hepatology News, is written by Nitin Ahuja, MD, and James Reynolds, MD, and provides an enlightening overview of the evaluation and management of chronic constipation. I hope that everyone enjoys this new format of The New Gastroenterologist. As always, if you have any feedback, have interest in contributing, or have ideas that you would like to hear about, please contact me ([email protected]) or Managing Editor Ryan Farrell ([email protected]).

Bryson W. Katona, MD, PhD
Editor in Chief of The New Gastroenterologist

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GI & Hepatology News is one of the most widely read publications focused on the gastroenterology community and is the official newspaper of the AGA. The New Gastroenterologist is the AGA publication targeted to trainees and early career physicians. Recognizing the strength of both digital and print communication, the AGA has consolidated its communication media.

John I. Allen, MD, MBA, AGAF
Editor in Chief of GI & Hepatology News

When The New Gastroenterologist debuted almost 3 years ago, it provided a mechanism for the AGA to condense and disseminate information in a single publication for those of us in training or in the early stages of our careers. Since then, The New Gastroenterologist has become a valuable resource for the AGA community and beyond. It is with great excitement that in 2018, The New Gastroenterologist will switch to a primarily digital format. Content will be distributed in quarterly e-newsletters, which will allow for easier distribution via social media. This will allow for the creation of a website archive of past articles that can be easily queried and accessed. Additionally, The New Gastroenterologist will debut an “In Focus” series of concise updates on pertinent topics in our field. These In Focus articles will be published on a quarterly basis in GI & Hepatology News and will undoubtedly be practical and informative features that will be of interest to all AGA members, regardless of their career stage. The first In Focus article, which appears in this issue of GI & Hepatology News, is written by Nitin Ahuja, MD, and James Reynolds, MD, and provides an enlightening overview of the evaluation and management of chronic constipation. I hope that everyone enjoys this new format of The New Gastroenterologist. As always, if you have any feedback, have interest in contributing, or have ideas that you would like to hear about, please contact me ([email protected]) or Managing Editor Ryan Farrell ([email protected]).

Bryson W. Katona, MD, PhD
Editor in Chief of The New Gastroenterologist

 

GI & Hepatology News is one of the most widely read publications focused on the gastroenterology community and is the official newspaper of the AGA. The New Gastroenterologist is the AGA publication targeted to trainees and early career physicians. Recognizing the strength of both digital and print communication, the AGA has consolidated its communication media.

John I. Allen, MD, MBA, AGAF
Editor in Chief of GI & Hepatology News

When The New Gastroenterologist debuted almost 3 years ago, it provided a mechanism for the AGA to condense and disseminate information in a single publication for those of us in training or in the early stages of our careers. Since then, The New Gastroenterologist has become a valuable resource for the AGA community and beyond. It is with great excitement that in 2018, The New Gastroenterologist will switch to a primarily digital format. Content will be distributed in quarterly e-newsletters, which will allow for easier distribution via social media. This will allow for the creation of a website archive of past articles that can be easily queried and accessed. Additionally, The New Gastroenterologist will debut an “In Focus” series of concise updates on pertinent topics in our field. These In Focus articles will be published on a quarterly basis in GI & Hepatology News and will undoubtedly be practical and informative features that will be of interest to all AGA members, regardless of their career stage. The first In Focus article, which appears in this issue of GI & Hepatology News, is written by Nitin Ahuja, MD, and James Reynolds, MD, and provides an enlightening overview of the evaluation and management of chronic constipation. I hope that everyone enjoys this new format of The New Gastroenterologist. As always, if you have any feedback, have interest in contributing, or have ideas that you would like to hear about, please contact me ([email protected]) or Managing Editor Ryan Farrell ([email protected]).

Bryson W. Katona, MD, PhD
Editor in Chief of The New Gastroenterologist

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Handshake

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There’s a simple act you’ve done with all your patients that you’ve probably been doing incorrectly. Yes, that is rather a bold assertion, but I’ll bet no one ever taught you the proper way. It’s only recently, after having done it thousands of times, that I came to realize there is a better way to give a handshake.

Handshakes come both at the critical first moment and at the close of patient interactions. The first helps establish who you are as a doctor and reassures your patient that you’re both capable and trustworthy. At the end of the visit, it seals the agreement wherein they commit to take your advice (or at least try) and you commit to do whatever necessary to help them.

high-number/Thinkstock

A poorly executed handshake, or worse, none at all, can erode trust or convey a lack of ability on your part. It’s true that handshakes aren’t always appropriate: For certain patients or disease states, they would be unsuitable. For the majority of patient visits, however, they are key. Here are some secrets to a good handshake:
 

  • As you’ve probably experienced, timing is critical. A handshake requires someone to anticipate your action and to coordinate perfectly with you. When you enter the room, move toward your patient and put your hand forward just as you approach your patient. Too early and you look like an awkward high schooler eager for a Justin Bieber autograph. Too late and you’ll take your patient by surprise. The best position is to have your left foot forward as you reach for their hand. This gives you stability and allows you to convey confidence.
  • As you approach your patient, make eye contact. Just a second or two as you cross the room is perfect. Then glance down at their now outstretched hand and connect web to web. Your arm should be tucked in and move straight toward their hand. Swinging out to come back in is great when you’re getting your new NBA jersey from the basketball commissioner, but not for getting patients comfortable with you.
  • The grip depends on the patient. For most adults, a firm squeeze with two arm pumps is just right. For the hard-charging, testosterone-replacing ex-Marine, you can reciprocate the extra-firm grasp – let him win the grip contest though, that’s what he wants. For the freezing-in-her-gown great grandmother, an extra long hold, sometimes even double handed, is fine, even appreciated.
  • No matter how firm, it is important to convey your enthusiasm and ability to your patient. This is done with a gentle push. As you shake hands, lightly push their arm back into them. This subtle transfer of energy from you to them is a little known tip that will make your handshake much more effective. Never push them off balance or worse, pull them toward you. Your objective is to create trust; making them unsteady will make that impossible.
  • Finally, let go after two pumps. If you feel them holding on, then stay until they release. For the majority of patients, that will be a just a couple seconds.

For patients I’ve never met, I often proffer my hand turned slightly upward for our first handshake. This subtle sign of submission shows I’m open and committed to them. For our closing handshake, I have my hand turned slightly downward so that my hand is slightly over theirs. This conveys that I’m confident in what I’ve said and done and that now I want them to uphold their part in our agreement.

I’ve been using the above technique for a few years now with success. It has helped with my patient satisfaction scores, and importantly, has helped me manage difficult patients for whom trust in our relationship is invaluable.

Dr. Jeffrey Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

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There’s a simple act you’ve done with all your patients that you’ve probably been doing incorrectly. Yes, that is rather a bold assertion, but I’ll bet no one ever taught you the proper way. It’s only recently, after having done it thousands of times, that I came to realize there is a better way to give a handshake.

Handshakes come both at the critical first moment and at the close of patient interactions. The first helps establish who you are as a doctor and reassures your patient that you’re both capable and trustworthy. At the end of the visit, it seals the agreement wherein they commit to take your advice (or at least try) and you commit to do whatever necessary to help them.

high-number/Thinkstock

A poorly executed handshake, or worse, none at all, can erode trust or convey a lack of ability on your part. It’s true that handshakes aren’t always appropriate: For certain patients or disease states, they would be unsuitable. For the majority of patient visits, however, they are key. Here are some secrets to a good handshake:
 

  • As you’ve probably experienced, timing is critical. A handshake requires someone to anticipate your action and to coordinate perfectly with you. When you enter the room, move toward your patient and put your hand forward just as you approach your patient. Too early and you look like an awkward high schooler eager for a Justin Bieber autograph. Too late and you’ll take your patient by surprise. The best position is to have your left foot forward as you reach for their hand. This gives you stability and allows you to convey confidence.
  • As you approach your patient, make eye contact. Just a second or two as you cross the room is perfect. Then glance down at their now outstretched hand and connect web to web. Your arm should be tucked in and move straight toward their hand. Swinging out to come back in is great when you’re getting your new NBA jersey from the basketball commissioner, but not for getting patients comfortable with you.
  • The grip depends on the patient. For most adults, a firm squeeze with two arm pumps is just right. For the hard-charging, testosterone-replacing ex-Marine, you can reciprocate the extra-firm grasp – let him win the grip contest though, that’s what he wants. For the freezing-in-her-gown great grandmother, an extra long hold, sometimes even double handed, is fine, even appreciated.
  • No matter how firm, it is important to convey your enthusiasm and ability to your patient. This is done with a gentle push. As you shake hands, lightly push their arm back into them. This subtle transfer of energy from you to them is a little known tip that will make your handshake much more effective. Never push them off balance or worse, pull them toward you. Your objective is to create trust; making them unsteady will make that impossible.
  • Finally, let go after two pumps. If you feel them holding on, then stay until they release. For the majority of patients, that will be a just a couple seconds.

For patients I’ve never met, I often proffer my hand turned slightly upward for our first handshake. This subtle sign of submission shows I’m open and committed to them. For our closing handshake, I have my hand turned slightly downward so that my hand is slightly over theirs. This conveys that I’m confident in what I’ve said and done and that now I want them to uphold their part in our agreement.

I’ve been using the above technique for a few years now with success. It has helped with my patient satisfaction scores, and importantly, has helped me manage difficult patients for whom trust in our relationship is invaluable.

Dr. Jeffrey Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

 

There’s a simple act you’ve done with all your patients that you’ve probably been doing incorrectly. Yes, that is rather a bold assertion, but I’ll bet no one ever taught you the proper way. It’s only recently, after having done it thousands of times, that I came to realize there is a better way to give a handshake.

Handshakes come both at the critical first moment and at the close of patient interactions. The first helps establish who you are as a doctor and reassures your patient that you’re both capable and trustworthy. At the end of the visit, it seals the agreement wherein they commit to take your advice (or at least try) and you commit to do whatever necessary to help them.

high-number/Thinkstock

A poorly executed handshake, or worse, none at all, can erode trust or convey a lack of ability on your part. It’s true that handshakes aren’t always appropriate: For certain patients or disease states, they would be unsuitable. For the majority of patient visits, however, they are key. Here are some secrets to a good handshake:
 

  • As you’ve probably experienced, timing is critical. A handshake requires someone to anticipate your action and to coordinate perfectly with you. When you enter the room, move toward your patient and put your hand forward just as you approach your patient. Too early and you look like an awkward high schooler eager for a Justin Bieber autograph. Too late and you’ll take your patient by surprise. The best position is to have your left foot forward as you reach for their hand. This gives you stability and allows you to convey confidence.
  • As you approach your patient, make eye contact. Just a second or two as you cross the room is perfect. Then glance down at their now outstretched hand and connect web to web. Your arm should be tucked in and move straight toward their hand. Swinging out to come back in is great when you’re getting your new NBA jersey from the basketball commissioner, but not for getting patients comfortable with you.
  • The grip depends on the patient. For most adults, a firm squeeze with two arm pumps is just right. For the hard-charging, testosterone-replacing ex-Marine, you can reciprocate the extra-firm grasp – let him win the grip contest though, that’s what he wants. For the freezing-in-her-gown great grandmother, an extra long hold, sometimes even double handed, is fine, even appreciated.
  • No matter how firm, it is important to convey your enthusiasm and ability to your patient. This is done with a gentle push. As you shake hands, lightly push their arm back into them. This subtle transfer of energy from you to them is a little known tip that will make your handshake much more effective. Never push them off balance or worse, pull them toward you. Your objective is to create trust; making them unsteady will make that impossible.
  • Finally, let go after two pumps. If you feel them holding on, then stay until they release. For the majority of patients, that will be a just a couple seconds.

For patients I’ve never met, I often proffer my hand turned slightly upward for our first handshake. This subtle sign of submission shows I’m open and committed to them. For our closing handshake, I have my hand turned slightly downward so that my hand is slightly over theirs. This conveys that I’m confident in what I’ve said and done and that now I want them to uphold their part in our agreement.

I’ve been using the above technique for a few years now with success. It has helped with my patient satisfaction scores, and importantly, has helped me manage difficult patients for whom trust in our relationship is invaluable.

Dr. Jeffrey Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

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