How Can Neurologists Treat Psychogenic Nonepileptic Seizures?

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Treatments, including CBT plus medication, have reduced seizures in randomized trials.

KANSAS CITY, MO—Many neurologists see, but few treat, patients with psychogenic nonepileptic seizures (PNES) and other conversion disorders, said W. Curt LaFrance Jr, MD, MPH, at the 46th Annual Meeting of the Child Neurology Society.

W. Curt LaFrance Jr, MD, MPH

PNES may be associated with stigma in the minds of neurologists and may require a shift in perspective. Once a diagnosis is made by a neurologist or epileptologist, a patient with PNES is usually referred to a psychiatrist, he said. “Many times, however, those patients are lost, falling between the gaps at the borderlands of neurology and psychiatry.”

Because treatments for PNES, including cognitive behavioral therapy (CBT)-informed psychotherapy, have reduced seizures in randomized clinical trials, neurologists can tell patients that there are ways to help them, said Dr. LaFrance. Dr. LaFrance is a dually-boarded neurologist and psychiatrist and is Director of Neuropsychiatry and Behavioral Neurology at Rhode Island Hospital and Associate Professor of Psychiatry and Neurology at the Warren Alpert Medical School of Brown University in Providence.

Diagnosing Conversion Disorder

PNES is a common, disabling, and costly disorder. Patients may see numerous providers and try numerous medications over time. Neurologists’ ability to distinguish between epileptic and nonepileptic seizures is essential. In addition, DSM-5 allows clinicians to diagnose conversion disorder based on the new criteria, which include documenting the presence of non-neuroanatomic signs.

Once neurologists have confirmed that a patient has PNES, they should not hedge their diagnosis or unnecessarily treat the patient with antiepileptic drugs (AEDs) if the patient has lone PNES. AEDs do not treat nonepileptic seizures, and neurologists may safely withdraw AEDs in patients with confirmed nonepileptic seizures who do not have an indication for an AED. “Once the diagnosis is made, in therapy, we then begin doing the hard work of getting to what lies underneath,” Dr. LaFrance said. “The conversion seizure or the psychogenic tremor is just the tip of the iceberg.”

Many patients have comorbid depression, anxiety, or personality disorders, and there is a high prevalence of abuse and trauma among children and adults with PNES. Effective treatment of PNES requires understanding the patient’s social context, and these developmental factors are “part of the history taking that we are responsible for in our exam as neurologists,” Dr. LaFrance said.

Wyllie et al found that about 80% of children with PNES were seizure-free at three years, compared with 40% of adults with PNES. In a study by Yadav et al, a third of young patients with PNES had resolution of symptoms by six months, while a third remained symptomatic at two years. Approaches to treatment for PNES have included conventional CBT, group and individual therapy, social interventions, physical and occupational therapy, medication, and treatment by neurologists and psychiatrists.

Therapeutic Trials

Dr. LaFrance and colleagues in 2010 published results from a pilot trial of an SSRI for the treatment of PNES. Patients ages 18 to 65 with video-EEG–confirmed PNES received sertraline or placebo over 12 weeks. Among the 33 patients included in an intent-to-treat analysis, those who received sertraline had a 45% reduction in seizure rate from baseline to final visit, compared with an 8% increase among patients in the placebo group. The study gave preliminary data for addressing comorbidities with PNES but was not powered to gauge the efficacy of an SSRI for PNES.

In a separate study published in 2009, Dr. LaFrance and colleagues evaluated the effect of CBT-informed psychotherapy in patients with PNES. Researchers treated participants at 12 weekly sessions using a manualized therapy. The treatment workbook had been modified from one originally developed as a psychotherapeutic intervention for aura identification and behavioral interventions to reduce epileptic seizures. In the open-label clinical trial, CBT-informed psychotherapy significantly reduced seizures, depression, and anxiety, and improved quality of life. Seizures initially increased, however, before decreasing during the therapy, which may reflect some of the psychological issues that patients are addressing, Dr. LaFrance said. Patients who had a reduction in seizures at the end of the pilot study maintained the reduction at one year.

This treatment approach is based on a theoretical fear-avoidance model in which patients have an injury or traumatic event and then develop PNES. They catastrophize, fear the next seizure, become hypervigilant to somatic cues, and avoid external environments. These factors create a “pattern of disuse, disability, and depression, and it becomes a vicious cycle,” Dr. LaFrance said. The goal of treatment is to give patients tools to enter a “virtuous cycle of confronting the fear and moving into recovery.”

A Multisite Study

The researchers then combined aspects of the pharmacologic and CBT trials in a 2014 multisite pilot randomized clinical trial that included the following four treatment arms: CBT-informed psychotherapy, medication (ie, flexible-dose sertraline hydrochloride), CBT-informed psychotherapy plus medication, and standard medical care (ie, biweekly assessments with a treating neurologist). Significant within-group seizure reduction occurred in the two arms receiving CBT-informed psychotherapy—a 51.4% weekly reduction with CBT-informed psychotherapy alone, and a 59.3% weekly reduction with CBT-informed psychotherapy plus sertraline. Patients’ quality of life and function also improved in the two therapy-containing arms. Sertraline reduced depression and showed a trend toward seizure reduction. Standard medical care did not significantly reduce seizures or improve secondary outcomes.

 

 

The research team is now examining neurocircuitry mechanisms of seizures with a recently funded multisite study of fMRI before and after treatment in patients with epilepsy or with PNES. Elements of the one-hour, CBT-informed psychotherapy sessions use different psychotherapeutic modalities, including motivational interviewing, interpersonal therapy, psychodynamic psychotherapy, distress tolerance, and psychoeducation about medications. Providers around the country, including neurologists, are being trained to deliver the intervention. “What we do is not rocket science. It is just good therapy,” Dr. LaFrance said.

—Jake Remaly

Suggested Reading

LaFrance WC Jr, Baird GL, Barry JJ, et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. JAMA Psychiatry. 2014;71(9):997-1005.

LaFrance WC Jr, Keitner GI, Papandonatos GD, et al. Pilot pharmacologic randomized controlled trial for psychogenic nonepileptic seizures. Neurology. 2010;75(13):1166-1173.

LaFrance WC Jr, Miller IW, Ryan CE, et al. Cognitive behavioral therapy for psychogenic nonepileptic seizures. Epilepsy Behav. 2009;14(4):591-596.

LaFrance WC Jr, Reuber M, Goldstein LH. Management of psychogenic nonepileptic seizures. Epilepsia. 2013;54 Suppl 1:53-67.

LaFrance Jr WC, Wincze JP. Treating Nonepileptic Seizures: Therapist Guide. New York, NY: Oxford University Press; 2015.

Reiter JM, Andrews D, Reiter C, LaFrance Jr WC. Taking Control of Your Seizures: Workbook. New York, NY: Oxford University Press; 2015.

Wyllie E, Friedman D, Lüders H, et al. Outcome of psychogenic seizures in children and adolescents compared with adults. Neurology. 1991;41(5):742-744.

Yadav A, Agarwal R, Park J. Outcome of psychogenic nonepileptic seizures (PNES) in children: A 2-year follow-up study. Epilepsy Behav. 2015;53:168-173.

Veterans Health Administration. Veterans and Epilepsy: Basic Training: Psychogenic Non-Epileptic Seizures [video]. YouTube. https://youtu.be/NlX-yNTX86w. Published February 27, 2017.

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Treatments, including CBT plus medication, have reduced seizures in randomized trials.
Treatments, including CBT plus medication, have reduced seizures in randomized trials.

KANSAS CITY, MO—Many neurologists see, but few treat, patients with psychogenic nonepileptic seizures (PNES) and other conversion disorders, said W. Curt LaFrance Jr, MD, MPH, at the 46th Annual Meeting of the Child Neurology Society.

W. Curt LaFrance Jr, MD, MPH

PNES may be associated with stigma in the minds of neurologists and may require a shift in perspective. Once a diagnosis is made by a neurologist or epileptologist, a patient with PNES is usually referred to a psychiatrist, he said. “Many times, however, those patients are lost, falling between the gaps at the borderlands of neurology and psychiatry.”

Because treatments for PNES, including cognitive behavioral therapy (CBT)-informed psychotherapy, have reduced seizures in randomized clinical trials, neurologists can tell patients that there are ways to help them, said Dr. LaFrance. Dr. LaFrance is a dually-boarded neurologist and psychiatrist and is Director of Neuropsychiatry and Behavioral Neurology at Rhode Island Hospital and Associate Professor of Psychiatry and Neurology at the Warren Alpert Medical School of Brown University in Providence.

Diagnosing Conversion Disorder

PNES is a common, disabling, and costly disorder. Patients may see numerous providers and try numerous medications over time. Neurologists’ ability to distinguish between epileptic and nonepileptic seizures is essential. In addition, DSM-5 allows clinicians to diagnose conversion disorder based on the new criteria, which include documenting the presence of non-neuroanatomic signs.

Once neurologists have confirmed that a patient has PNES, they should not hedge their diagnosis or unnecessarily treat the patient with antiepileptic drugs (AEDs) if the patient has lone PNES. AEDs do not treat nonepileptic seizures, and neurologists may safely withdraw AEDs in patients with confirmed nonepileptic seizures who do not have an indication for an AED. “Once the diagnosis is made, in therapy, we then begin doing the hard work of getting to what lies underneath,” Dr. LaFrance said. “The conversion seizure or the psychogenic tremor is just the tip of the iceberg.”

Many patients have comorbid depression, anxiety, or personality disorders, and there is a high prevalence of abuse and trauma among children and adults with PNES. Effective treatment of PNES requires understanding the patient’s social context, and these developmental factors are “part of the history taking that we are responsible for in our exam as neurologists,” Dr. LaFrance said.

Wyllie et al found that about 80% of children with PNES were seizure-free at three years, compared with 40% of adults with PNES. In a study by Yadav et al, a third of young patients with PNES had resolution of symptoms by six months, while a third remained symptomatic at two years. Approaches to treatment for PNES have included conventional CBT, group and individual therapy, social interventions, physical and occupational therapy, medication, and treatment by neurologists and psychiatrists.

Therapeutic Trials

Dr. LaFrance and colleagues in 2010 published results from a pilot trial of an SSRI for the treatment of PNES. Patients ages 18 to 65 with video-EEG–confirmed PNES received sertraline or placebo over 12 weeks. Among the 33 patients included in an intent-to-treat analysis, those who received sertraline had a 45% reduction in seizure rate from baseline to final visit, compared with an 8% increase among patients in the placebo group. The study gave preliminary data for addressing comorbidities with PNES but was not powered to gauge the efficacy of an SSRI for PNES.

In a separate study published in 2009, Dr. LaFrance and colleagues evaluated the effect of CBT-informed psychotherapy in patients with PNES. Researchers treated participants at 12 weekly sessions using a manualized therapy. The treatment workbook had been modified from one originally developed as a psychotherapeutic intervention for aura identification and behavioral interventions to reduce epileptic seizures. In the open-label clinical trial, CBT-informed psychotherapy significantly reduced seizures, depression, and anxiety, and improved quality of life. Seizures initially increased, however, before decreasing during the therapy, which may reflect some of the psychological issues that patients are addressing, Dr. LaFrance said. Patients who had a reduction in seizures at the end of the pilot study maintained the reduction at one year.

This treatment approach is based on a theoretical fear-avoidance model in which patients have an injury or traumatic event and then develop PNES. They catastrophize, fear the next seizure, become hypervigilant to somatic cues, and avoid external environments. These factors create a “pattern of disuse, disability, and depression, and it becomes a vicious cycle,” Dr. LaFrance said. The goal of treatment is to give patients tools to enter a “virtuous cycle of confronting the fear and moving into recovery.”

A Multisite Study

The researchers then combined aspects of the pharmacologic and CBT trials in a 2014 multisite pilot randomized clinical trial that included the following four treatment arms: CBT-informed psychotherapy, medication (ie, flexible-dose sertraline hydrochloride), CBT-informed psychotherapy plus medication, and standard medical care (ie, biweekly assessments with a treating neurologist). Significant within-group seizure reduction occurred in the two arms receiving CBT-informed psychotherapy—a 51.4% weekly reduction with CBT-informed psychotherapy alone, and a 59.3% weekly reduction with CBT-informed psychotherapy plus sertraline. Patients’ quality of life and function also improved in the two therapy-containing arms. Sertraline reduced depression and showed a trend toward seizure reduction. Standard medical care did not significantly reduce seizures or improve secondary outcomes.

 

 

The research team is now examining neurocircuitry mechanisms of seizures with a recently funded multisite study of fMRI before and after treatment in patients with epilepsy or with PNES. Elements of the one-hour, CBT-informed psychotherapy sessions use different psychotherapeutic modalities, including motivational interviewing, interpersonal therapy, psychodynamic psychotherapy, distress tolerance, and psychoeducation about medications. Providers around the country, including neurologists, are being trained to deliver the intervention. “What we do is not rocket science. It is just good therapy,” Dr. LaFrance said.

—Jake Remaly

Suggested Reading

LaFrance WC Jr, Baird GL, Barry JJ, et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. JAMA Psychiatry. 2014;71(9):997-1005.

LaFrance WC Jr, Keitner GI, Papandonatos GD, et al. Pilot pharmacologic randomized controlled trial for psychogenic nonepileptic seizures. Neurology. 2010;75(13):1166-1173.

LaFrance WC Jr, Miller IW, Ryan CE, et al. Cognitive behavioral therapy for psychogenic nonepileptic seizures. Epilepsy Behav. 2009;14(4):591-596.

LaFrance WC Jr, Reuber M, Goldstein LH. Management of psychogenic nonepileptic seizures. Epilepsia. 2013;54 Suppl 1:53-67.

LaFrance Jr WC, Wincze JP. Treating Nonepileptic Seizures: Therapist Guide. New York, NY: Oxford University Press; 2015.

Reiter JM, Andrews D, Reiter C, LaFrance Jr WC. Taking Control of Your Seizures: Workbook. New York, NY: Oxford University Press; 2015.

Wyllie E, Friedman D, Lüders H, et al. Outcome of psychogenic seizures in children and adolescents compared with adults. Neurology. 1991;41(5):742-744.

Yadav A, Agarwal R, Park J. Outcome of psychogenic nonepileptic seizures (PNES) in children: A 2-year follow-up study. Epilepsy Behav. 2015;53:168-173.

Veterans Health Administration. Veterans and Epilepsy: Basic Training: Psychogenic Non-Epileptic Seizures [video]. YouTube. https://youtu.be/NlX-yNTX86w. Published February 27, 2017.

KANSAS CITY, MO—Many neurologists see, but few treat, patients with psychogenic nonepileptic seizures (PNES) and other conversion disorders, said W. Curt LaFrance Jr, MD, MPH, at the 46th Annual Meeting of the Child Neurology Society.

W. Curt LaFrance Jr, MD, MPH

PNES may be associated with stigma in the minds of neurologists and may require a shift in perspective. Once a diagnosis is made by a neurologist or epileptologist, a patient with PNES is usually referred to a psychiatrist, he said. “Many times, however, those patients are lost, falling between the gaps at the borderlands of neurology and psychiatry.”

Because treatments for PNES, including cognitive behavioral therapy (CBT)-informed psychotherapy, have reduced seizures in randomized clinical trials, neurologists can tell patients that there are ways to help them, said Dr. LaFrance. Dr. LaFrance is a dually-boarded neurologist and psychiatrist and is Director of Neuropsychiatry and Behavioral Neurology at Rhode Island Hospital and Associate Professor of Psychiatry and Neurology at the Warren Alpert Medical School of Brown University in Providence.

Diagnosing Conversion Disorder

PNES is a common, disabling, and costly disorder. Patients may see numerous providers and try numerous medications over time. Neurologists’ ability to distinguish between epileptic and nonepileptic seizures is essential. In addition, DSM-5 allows clinicians to diagnose conversion disorder based on the new criteria, which include documenting the presence of non-neuroanatomic signs.

Once neurologists have confirmed that a patient has PNES, they should not hedge their diagnosis or unnecessarily treat the patient with antiepileptic drugs (AEDs) if the patient has lone PNES. AEDs do not treat nonepileptic seizures, and neurologists may safely withdraw AEDs in patients with confirmed nonepileptic seizures who do not have an indication for an AED. “Once the diagnosis is made, in therapy, we then begin doing the hard work of getting to what lies underneath,” Dr. LaFrance said. “The conversion seizure or the psychogenic tremor is just the tip of the iceberg.”

Many patients have comorbid depression, anxiety, or personality disorders, and there is a high prevalence of abuse and trauma among children and adults with PNES. Effective treatment of PNES requires understanding the patient’s social context, and these developmental factors are “part of the history taking that we are responsible for in our exam as neurologists,” Dr. LaFrance said.

Wyllie et al found that about 80% of children with PNES were seizure-free at three years, compared with 40% of adults with PNES. In a study by Yadav et al, a third of young patients with PNES had resolution of symptoms by six months, while a third remained symptomatic at two years. Approaches to treatment for PNES have included conventional CBT, group and individual therapy, social interventions, physical and occupational therapy, medication, and treatment by neurologists and psychiatrists.

Therapeutic Trials

Dr. LaFrance and colleagues in 2010 published results from a pilot trial of an SSRI for the treatment of PNES. Patients ages 18 to 65 with video-EEG–confirmed PNES received sertraline or placebo over 12 weeks. Among the 33 patients included in an intent-to-treat analysis, those who received sertraline had a 45% reduction in seizure rate from baseline to final visit, compared with an 8% increase among patients in the placebo group. The study gave preliminary data for addressing comorbidities with PNES but was not powered to gauge the efficacy of an SSRI for PNES.

In a separate study published in 2009, Dr. LaFrance and colleagues evaluated the effect of CBT-informed psychotherapy in patients with PNES. Researchers treated participants at 12 weekly sessions using a manualized therapy. The treatment workbook had been modified from one originally developed as a psychotherapeutic intervention for aura identification and behavioral interventions to reduce epileptic seizures. In the open-label clinical trial, CBT-informed psychotherapy significantly reduced seizures, depression, and anxiety, and improved quality of life. Seizures initially increased, however, before decreasing during the therapy, which may reflect some of the psychological issues that patients are addressing, Dr. LaFrance said. Patients who had a reduction in seizures at the end of the pilot study maintained the reduction at one year.

This treatment approach is based on a theoretical fear-avoidance model in which patients have an injury or traumatic event and then develop PNES. They catastrophize, fear the next seizure, become hypervigilant to somatic cues, and avoid external environments. These factors create a “pattern of disuse, disability, and depression, and it becomes a vicious cycle,” Dr. LaFrance said. The goal of treatment is to give patients tools to enter a “virtuous cycle of confronting the fear and moving into recovery.”

A Multisite Study

The researchers then combined aspects of the pharmacologic and CBT trials in a 2014 multisite pilot randomized clinical trial that included the following four treatment arms: CBT-informed psychotherapy, medication (ie, flexible-dose sertraline hydrochloride), CBT-informed psychotherapy plus medication, and standard medical care (ie, biweekly assessments with a treating neurologist). Significant within-group seizure reduction occurred in the two arms receiving CBT-informed psychotherapy—a 51.4% weekly reduction with CBT-informed psychotherapy alone, and a 59.3% weekly reduction with CBT-informed psychotherapy plus sertraline. Patients’ quality of life and function also improved in the two therapy-containing arms. Sertraline reduced depression and showed a trend toward seizure reduction. Standard medical care did not significantly reduce seizures or improve secondary outcomes.

 

 

The research team is now examining neurocircuitry mechanisms of seizures with a recently funded multisite study of fMRI before and after treatment in patients with epilepsy or with PNES. Elements of the one-hour, CBT-informed psychotherapy sessions use different psychotherapeutic modalities, including motivational interviewing, interpersonal therapy, psychodynamic psychotherapy, distress tolerance, and psychoeducation about medications. Providers around the country, including neurologists, are being trained to deliver the intervention. “What we do is not rocket science. It is just good therapy,” Dr. LaFrance said.

—Jake Remaly

Suggested Reading

LaFrance WC Jr, Baird GL, Barry JJ, et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. JAMA Psychiatry. 2014;71(9):997-1005.

LaFrance WC Jr, Keitner GI, Papandonatos GD, et al. Pilot pharmacologic randomized controlled trial for psychogenic nonepileptic seizures. Neurology. 2010;75(13):1166-1173.

LaFrance WC Jr, Miller IW, Ryan CE, et al. Cognitive behavioral therapy for psychogenic nonepileptic seizures. Epilepsy Behav. 2009;14(4):591-596.

LaFrance WC Jr, Reuber M, Goldstein LH. Management of psychogenic nonepileptic seizures. Epilepsia. 2013;54 Suppl 1:53-67.

LaFrance Jr WC, Wincze JP. Treating Nonepileptic Seizures: Therapist Guide. New York, NY: Oxford University Press; 2015.

Reiter JM, Andrews D, Reiter C, LaFrance Jr WC. Taking Control of Your Seizures: Workbook. New York, NY: Oxford University Press; 2015.

Wyllie E, Friedman D, Lüders H, et al. Outcome of psychogenic seizures in children and adolescents compared with adults. Neurology. 1991;41(5):742-744.

Yadav A, Agarwal R, Park J. Outcome of psychogenic nonepileptic seizures (PNES) in children: A 2-year follow-up study. Epilepsy Behav. 2015;53:168-173.

Veterans Health Administration. Veterans and Epilepsy: Basic Training: Psychogenic Non-Epileptic Seizures [video]. YouTube. https://youtu.be/NlX-yNTX86w. Published February 27, 2017.

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Guidance for the Clinical Management of Thirdhand Smoke Exposure in the Child Health Care Setting

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From the Center for Child and Adolescent Health Research and Policy, Division of General Academic Pediatrics, Massachusetts General Hospital for Children, and the Tobacco Research and Treatment Center, Massachusetts General Hospital, Boston, MA.

 

Abstract

  • Objective: To explain the concept of thirdhand smoke and how it can be used to protect the health of children and improve delivery of tobacco control interventions for parents in the child health care setting.
  • Methods: Review of the literature and descriptive report.
  • Results: The thirdhand smoke concept has been used in the CEASE intervention to improve the delivery of tobacco control counseling and services to parents. Materials and techniques have been developed for the child health care setting that use the concept of thirdhand smoke. Scientific findings demonstrate that thirdhand smoke exposure is harmful and establishes the need for clinicians to communicate the cessation imperative: the only way to protect non-smoking household members from thirdhand smoke is for all household smokers to quit smoking completely. As the scientific knowledge of thirdhand smoke increases, advocates will likely rely on it to encourage completely smoke-free places.
  • Conclusion: Recent scientific studies on thirdhand smoke are impelling further research on the topic, spurring the creation of tobacco control policies to protect people from thridhand smoke and stimulating improvements to the delivery of tobacco control counseling and services to parents in child health care settings.

Key words: thirdhand smoke; smoking; tobacco; indoor air quality; smoking cessation; pediatrics.

 

While “thirdhand smoke” may be a relatively new term, it is rooted in an old concept—the particulate matter and residue from tobacco smoke left behind after tobacco is burned. In 1953, Dr. Ernest Wynder and his colleagues from the Washington University School of Medicine in St. Louis showed that condensate made from the residue of cigarette smoke causes cancer [1]. This residue left behind by burning cigarettes is now known as thirdhand smoke [2]. Dr. Wynder used acetone to rinse the leftover tobacco smoke residue from a smoking chamber where he had burned cigarettes. He then painted the solution of acetone and thirdhand smoke residue onto the backs of mice. The results of Dr. Wynder’s study demonstrated that exposed mice developed cancerous skin lesions, whereas mice exposed to the acetone alone did not display skin lesions. Dr. Wynder sounded an alarm bell in his manuscript when he wrote, “Such studies, in view of the corollary clinical data relating smoking to various types of cancer, appear urgent. They may result not only in furthering our knowledge of carcinogenesis, but in promoting some practical aspects of cancer prevention [1].”

Decades of research has been conducted since Dr. Wynder’s discovery to definitively conclude that smoking tobacco and exposure to secondhand tobacco smoke is harmful to human health. It is estimated that 480,000 annual premature deaths in the United States alone are attributable to smoking and exposure to secondhand smoke [3]. The World Health Organization estimates that worldwide tobacco use is responsible for more than 7 million deaths per year, with 890,000 of those deaths caused by secondhand smoke exposure of nonsmokers [4]. Epidemiological evidence of the harm posed by tobacco has spurred the U.S Surgeon General to conclude that there is no risk-free level of exposure to tobacco smoke [5]. Despite the overwhelming evidence implicating tobacco as the cause of an unprecedented amount of disease resulting from the use of a consumer product, only recently has a dedicated research agenda been pursued to study what Dr. Wynder urgently called for back in 1953: further exploration of the health effects of thirdhand tobacco smoke.

The term "thirdhand smoke" was first coined in 2006 by researchers with the Clinical Effort Against Secondhand Smoke Exposure (CEASE) program at Massachusetts General Hospital in Boston [6], and recent research has begun to shed considerable light on the topic. In 2011, a research consortium of scientists funded by the Tobacco-Related Disease Research Program [7] in California was set up to conduct pioneering research on the characterization, exposure and health effects of thirdhand tobacco smoke [8]. Research findings from this consortium and other scientists from around the world are quickly expanding and disseminating knowledge on this important topic.

While the research on thirdhand smoke is ongoing, this paper summarizes the current literature most relevant to the pediatric population and outlines clinical and policy recommendations to protect children and families from the harms of exposure to thirdhand smoke.

What Is Thirdhand Smoke and How Is It Different from Secondhand Smoke?

Thirdhand smoke is a result of combusted tobacco, most often from smoking cigarettes, pipes, cigars, or cigarillos. Thirdhand smoke remains on surfaces and in dust for a longtime after smoking happens, reacts with oxidants and other compounds to form secondary pollutants, and is re-emitted as a gas and/or resuspended when particles are disturbed and go back into the air where they can be inhaled [9]. One dramatic example of how thirdhand smoke can remain on surfaces long after secondhand smoke dissipates was discovered on the ornate constellation ceiling in the main concourse of the Grand Central Terminal in New York City. According to Sam Roberts, a correspondent for the New York Times and the author of a book about the historic train station, the dark residue that accumulated on the concourse ceiling over decades and was originally believed to be the result of soot from train engines was primarily residue from tobacco smoke [10–12]. It wasn’t until a restoration in the 1990s when workers scrubbed the tar and nicotine residue from the ceiling could the elaborate design of the zodiac signs and constellations be seen again [13]. A similar process takes place inside homes, where smoke residue accumulates on surfaces such as walls and ceilings after smoking happens. Owners of homes that have been previously smoked in are faced with unanswered questions about how to clean up the toxic substances left behind.

When tobacco is smoked, the particulates contained in secondhand smoke settle on surfaces; this contamination is absorbed deep into materials such as hair, clothes, carpeting, furniture, and wallboard [9,14]. After depositing onto surfaces, the chemicals undergo an aging process, which changes the chemical structure of the smoke pollutants. The nicotine in thirdhand smoke residue reacts with common indoor air pollutants, such as nitrous acid and ozone, to form hazardous substances. When the nicotine present in thirdhand smoke reacts with nitrous acid, it forms carcinogenic tobacco-specific nitrosamines such as NNK and NNN [15–17]. Nicotine also reacts with ozone to form additional harmful ultrafine particles that can embed deep within the lungs when inhaled [18]. As thirdhand smoke ages, it becomes more toxic [15]. The aged particles then undergo a process called “off-gassing,” in which gas is continuously re-emitted from these surfaces back into the air [19]. This process of off-gassing occurs long after cigarettes have been smoked indoors [19,20]. Thirdhand smoke particles can also be inhaled when they get resuspended into the air after contaminated surfaces are disturbed [21].

Common practices employed by smokers, like smoking in different rooms, using fans to diffuse the smoke, or opening windows, do not prevent the formation and inhalation of thirdhand smoke by people living or visiting these indoor spaces [22]. Environments with potential thirdhand smoke exposure include homes of smokers [23], apartments and homes previously occupied by smokers [24], multiunit housing where smoking is permitted [25], automobiles that have been smoked in [26], hotel rooms where smoking is permitted [27], and other indoor places where smoking has occurred.

Research Supports Having Completely Smoke-Free Environments

Recent research has shown that exposure to thirdhand smoke is harmful. These findings, many of which are described below, offer strong support in favor of advocating for environments free of thirdhand smoke contamination for families and children.

Genetic Damage from Thirdhand Smoke Exposure

In 2013, researchers from the Lawrence Berkeley National Laboratory were the first to demonstrate that thirdhand smoke causes significant genetic damage to human cells [28]. Using in vitro assays, the researchers showed that thirdhand smoke is a cause of harm to human DNA in the form of strand breaks and oxidative damage, which leads to mutations that can cause cancer. The researches also specifically tested the effect of NNA, a tobacco-specific nitrosamine that is commonly found in thirdhand smoke but not in secondhand smoke, on human cell cultures and found that it caused significant damage to DNA [28].

Children Show Elevated Biomarkers of Thirdhand Smoke Exposure in Their Urine and Hair Samples

In 2004, Matt and colleagues described how they collected household dust samples from living rooms and infants’ bedrooms [23]. Their research demonstrated that nicotine accumulated on the living room and infants’ bedroom surfaces of the homes belonging to smokers. Significantly higher amounts of urine cotinine, a biomarker for exposure to nicotine, were detected among infants who lived in homes where smoking happens inside compared to homes where smokers go outside to smoke [23]. As well, a study published in 2017 that measured the presence of hand nicotine on children of smokers who presented to the emergency room for an illness possibly related to tobacco smoke exposure detected hand nicotine on the hands of each child who participated in this pilot study. The researchers found a positive correlation between the amount of nicotine found on children’s hands and the amount of cotinine, a biomarker for nicotine exposure, detected in the children’s saliva [29].

Children Are Exposed to Higher Ratios of Thirdhand Smoke than Adults

In 2009, researchers discovered that the thirdhand smoke ratio of tobacco-specific nitrosamines to nicotine increases during the aging process [9]. Biomarkers measured in the urine can now be used to estimate the degree to which people have been exposed to secondhand or thirdhand smoke based on the ratio of the thirdhand smoke biomarker NNK and nicotine. Toddlers who live with adults who smoke have higher NNK/nicotine ratios, suggesting that they are exposed to a higher ratio of thirdhand smoke compared to secondhand smoke than adults [30]. Young children are likely exposed to higher ratios of thirdhand smoke as they spend more time on the floor, where thirdhand smoke accumulates. They frequently put their hands and other objects into their mouths. Young children breathe faster than adults, increasing their inhalation exposure and also have thinner skin, making dermal absorption more efficient [9].

Modeling Excess Cancer Risk

A 2014 United Kingdom study used official sources of toxicological data about chemicals detected in thirdhand smoke–contaminated homes to assess excess cancer risk posed from thirdhand smoke [17]. Using dust samples collected from homes where a smoker lived, they estimate that the median lifetime excess cancer risk from the exposure to all the nitrosamines present in thirdhand smoke is 9.6 additional cancer cases per 100,000 children exposed and could be as high as 1 excess cancer case per 1000 children exposed. The researchers concluded that young children aged 1 to 6 are at an especially increased risk for cancer because of their frequent contact with surfaces contaminated with thirdhand smoke and their ingestion of the particulate matter that settles on surfaces after smoking takes place [17].

 

 

Infants in Health Care Facilities Are Exposed to Thirdhand Smoke

Researchers have observed biomarkers confirming thirdhand smoke exposure in the urine of infants in the NICU. Found in incubators and cribs, particulates are likely being deposited in the NICU from visitors who have thirdhand smoke on their clothing, skin, and hair [31].

Animal Studies Link Thirdhand Smoke Exposure to Common Human Disease

Mice exposed to thirdhand smoke under conditions meant to simulate levels similar to human exposure are pre-diabetic, are at higher risk of developing metabolic syndrome, have inflammatory markers in the lungs that increase the risk for asthma, show slow wound healing, develop nonalcoholic fatty liver disease, and become behaviorally hyperactive [32]. Another recent study published in 2017 showed that mice exposed to thirdhand smoke after birth weighed less than mice not exposed to thirdhand smoke. Additionally, mice exposed to thirdhand smoke early in life showed changes in white blood cell counts that persisted into adulthood [9,33].

Summary

In summary, recent research makes a compelling case for invoking the precautionary principle to ensure that children avoid exposures to thirdhand smoke in their homes, cars, and healthcare settings. Studies reveal that:

  • children live in homes where thirdhand smoke is present and this exposure is detectable in their bodies [23]
  • concentrations of thirdhand smoke exposure observed in children are disproportionately higher than adults [30]
  • chemicals present in thirdhand smoke cause damage to DNA [28]
  • thirdhand smoke contains carcinogens that put exposed children at increased risk of cancer [17]
  • thirdhand smoke is being detected within medical settings [34] and in the bodies of medically-vulnerable children [29], and
  • animal studies have linked exposure to thirdhand smoke to a number of adverse health conditions commonly seen in today’s pediatric population such as metabolic syndrome, prediabetes, asthma, hyperactivity [32] and low birth weight [33].

Using the Thirdhand Smoke Concept in Clinical Practice

The clinical setting is an ideal place to address thirdhand smoke with families as a component of a comprehensive tobacco control strategy.

The Cessation Imperative—A Novel Motivational Message Prompted by Thirdhand Smoke

While there are potentially many ways to address thirdhand smoke exposure with families, the CEASE program has been used in the primary care setting to train child health care clinicians and office staff to address second- and thirdhand smoke. The training also educates clinicians on providing cessation counseling and resources to families with the goal of helping all family members become tobacco free, as well as to helping families keep completely smoke-free homes and cars [35,36]. The concept of thirdhand smoke creates what we have coined the cessation imperative [36]. The cessation imperative is based on the notion that the only way to protect non-smoking family and household members from thirdhand smoke is for all household smokers to quit smoking completely. Smoking, even when not in the presence of children, can expose others to toxic contaminates that settle on the surfaces of the home, the car as well as to the skin, hair, and clothing of family members who smoke. A discussion with parents about eliminating only secondhand smoke exposure for children does not adequately address how continued smoking, even when children are not present, can be harmful. The thirdhand smoke concept can be presented early, making it an efficient way to advocate for completely smoke-free families.

Thirdhand Smoke Counseling Helps Clinicians Achieve Key Tobacco Control Goals

The American Academy of Pediatrics (AAP) and the American Academy of Family Physicians (AAFP) recommend that health care providers deliver advice to parents regarding establishing smoke-free homes and cars and provide information about how their smoking adversely affects their children’s health [37,38]. It is AAP and AAFP policy that health care providers provide tobacco dependence treatment and referral to cessation services to help adult family members quit smoking [38,39]. Successfully integrating counseling around the topic of thirdhand smoke into existing smoking cessation service delivery is possible. The CEASE research and implementation team developed and disseminated educational content to clinicians about thirdhand smoke through AAP courses delivered online [40] as well as made presentations to clinicians at AAP-sponsored training sessions. Thirdhand smoke messaging has been included in the CEASE practice trainings so that participating clinicians in pediatric offices are equipped to engage parents on this topic. Further information about these educational resources and opportunities can be obtained from the AAP Julius B. Richmond Center of Excellence website [41] and from the Massachusetts General Hospital CEASE program’s website [42].

Counseling parents about thirdhand smoke can help assist parents with their smoking in the critical context of their child’s care. Most parents see their child’s health care clinician more often than their own [43]. Increasing the number of pediatric clinical encounters where parental smoking is addressed while also increasing the effectiveness of these clinical encounters by increasing parents’ motivation to protect their children from tobacco smoke exposure are important goals. The topic of thirdhand smoke is a novel concept that clinicians can use to engage with parents around their smoking in a new way. Recent research conducted by the CEASE team suggests that counseling parents in the pediatric setting about thirdhand smoke can be useful in helping achieve tobacco control goals with families. Parent’s belief about thirdhand smoke is associated with the likelihood the parent will take concrete steps to protect their child. Parents who believe thirdhand smoke is harmful are more likely to protect their children from exposure by adopting strictly enforced smoke-free home and car rules [44]. Parents who changed their thirdhand smoke beliefs over the course of a year to believing that thirdhand smoke is harmful were more likely to try to quit smoking [44].

Child health care clinicians are effective at influencing parents’ beliefs about the potential harm thirdhand smoke poses to their children. Parents who received advice from pediatricians to quit smoking or to adopt smoke-free home or policies were more likely to believe that thirdhand smoke was harmful to the health of children [45]. Fathers (as compared with mothers) and parents who smoked more cigarettes each day were less likely to accept that thirdhand smoke is harmful to children [45]. Conversely, delivering effective educational messages and counseling around the topic of thirdhand smoke to parents may help promote smoke-free rules and acceptance of cessation assistance.

 

 

Protect Patients from Thirdhand Smoke Risks

All health care settings should be completely smoke-free. Smoking bans help protect all families and children from second and thirdhand smoke exposure. It is especially important for medically vulnerable children to visit facilities free from all forms of tobacco smoke contamination. CEASE trainings encourage practices to implement a zone of wellness on the grounds of the healthcare facility by completely banning smoking. The CEASE implementation team also trains practice leaders to reach out to all staff that use tobacco and offer resources and support for quitting. Having a non-smoking staff sets a great example for families who visit the healthcare facility, and reduces the likelihood of bringing thirdhand smoke contaminates into the facility. Creating a policy that addresses thirdhand smoke exposure is a concrete step that health care organizations can take to protect patients.

Thirdhand Smoke Resources Developed and/or Used by the CEASE Program

The CEASE program has developed and/or identified a number of clinical resources to educate parents and clinicians about thirdhand smoke. These free resources can enhance awareness of thirdhand smoke and help promote the use of the thirdhand smoke concept in clinical practice.

  • Posters with messages designed to educate parents about thirdhand smoke to encourage receipt of cessation resources were created for use in waiting areas and exam rooms of child health care practices. A poster for clinical practice (Figure 1) can be downloaded and printed from the CEASE program website [42].
  • Health education handouts that directly address thirdhand smoke exposure are available. The handouts can be taken home to family members who are not present at the visit and contain the telephone number for the tobacco quitline service, which connects smokers in the United States with free telephone support for smoking cessation. Handouts for clinical practice can be downloaded and printed from the CEASE program website. Figure 2 shows a handout that encourages parents to keep a smoke-free car by pointing out that tobacco smoke stays in the car long after the cigarette is out.
  • Videos about thirdhand smoke can be viewed by parents while in child health care offices or shared on practice websites or social media platforms. The CEASE program encourages practices to distribute videos about thirdhand smoke to introduce parents to the concept of thirdhand smoke and to encourage parents to engage in a discussion with their child’s clinicians about ways to limit thirdhand smoke exposure. Suitable videos for parental viewing include the 2 listed below, which highlight information from the Thirdhand Smoke Research Consortium.
      -University of California Riverside https://youtu.be/i1rhqRy-2e8
     -San Diego State University https://youtu.be/rqzi-9sXLdU
  • Letters for landlords and management companies were created to stress the importance of providing a smoke-free living environment for children. The letters are meant to be signed by the child’s health care provider. The letters state that eliminating smoking in their buildings would result in landlords that “Pay less for cleaning and turnover fees.” Landlord letter templates can be downloaded and printed from the CEASE program website [42].
  • Educational content for child health care clinicians about thirdhand smoke and how to counsel parents is included in the American Academy of Pediatrics Education in Quality Improvement for Pediatric Practice (EQIPP) online course entitled “Eliminating Tobacco” Use and Exposure to Secondhand Smoke. A section devoted to educating clinicians on the topic of thirdhand smoke is presented in this course. The course can be accessed through the AAP website and it qualifies for American Board of Pediatrics maintenance of certification part IV credit [40].

The CEASE team has worked with mass media outlets to communicate the messages about thirdhand smoke to build public awareness. The Today Show helped to popularize the concept of thirdhand smoke in 2009 after a paper published in the journal Pediatrics linked thirdhand smoke beliefs to home smoking bans [2].

 

 

Systems Approaches to Reduce Thirdhand Smoke Exposure

Public Policy Approaches

A clear policy agenda can help people protect their families from exposure to thirdhand smoke [46]. Policy approaches that have worked for lead, asbestos, and radon are examples of common household contaminants that are regulated using different mechanisms in an effort to protect the public health [46]. Strengths and weaknesses in each of these different approaches should be carefully considered when developing a comprehensive policy agenda to address thirdhand smoke. Recently, research on the health effects of thirdhand smoke spurred the passage of California legislative bill AB 1819 that “prohibits smoking tobacco at all times in the homes of licensed family child care homes and in areas where children are present [47].” As well, a recent US Department of Housing and Urban Development rule was finalized that requires all public housing agencies to implement a smoke-free policy by 30 July 2018 [48]. Smoke-free housing protects occupants from both secondhand and thirdhand smoke exposure. Pediatricians and other child health care professionals are well positioned to advocate for legislative actions that protect children from harmful exposures to thirdhand smoke.

Practice Change in Child Health Care Settings

Designing health care systems to screen for tobacco smoke exposure and to provide evidence-based cessation resources for all smokers is one of the best ways to reduce exposures to thirdhand smoke. Preventing thirdhand smoke exposure can work as novel messaging to promote tobacco cessation programs. Developing electronic medical record systems that allow for documentation of the smoking status of household members and whether or not homes and cars are completely smokefree can be particularly helpful tools for child health care providers when addressing thirdhand smoke with families. Good documentation about smoke-free homes and cars can enhance follow-up discussions with families as they work towards reducing thirdhand smoke exposures.

Summary

The thirdhand smoke concept has been used to improve delivery of tobacco control counseling and services for parents in the child health care context. Free materials are available that utilize thirdhand smoke messaging. As the science of thirdhand smoke matures, it will increasingly be used to help promote completely smoke-free places. The existing research on thirdhand smoke establishes the need for clinicians to communicate the cessation imperative. By using it, clinicians can help all smokers and non-smokers understand that there is no way to smoke tobacco without exposing friends and family.

 

Corresponding author: Jeremy E. Drehmer, MPH, 125 Nashua St., Suite 860, Boston, MA 02114, jdrehmer@ mgh.harvard.edu.

Financial disclosures: None

References

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From the Center for Child and Adolescent Health Research and Policy, Division of General Academic Pediatrics, Massachusetts General Hospital for Children, and the Tobacco Research and Treatment Center, Massachusetts General Hospital, Boston, MA.

 

Abstract

  • Objective: To explain the concept of thirdhand smoke and how it can be used to protect the health of children and improve delivery of tobacco control interventions for parents in the child health care setting.
  • Methods: Review of the literature and descriptive report.
  • Results: The thirdhand smoke concept has been used in the CEASE intervention to improve the delivery of tobacco control counseling and services to parents. Materials and techniques have been developed for the child health care setting that use the concept of thirdhand smoke. Scientific findings demonstrate that thirdhand smoke exposure is harmful and establishes the need for clinicians to communicate the cessation imperative: the only way to protect non-smoking household members from thirdhand smoke is for all household smokers to quit smoking completely. As the scientific knowledge of thirdhand smoke increases, advocates will likely rely on it to encourage completely smoke-free places.
  • Conclusion: Recent scientific studies on thirdhand smoke are impelling further research on the topic, spurring the creation of tobacco control policies to protect people from thridhand smoke and stimulating improvements to the delivery of tobacco control counseling and services to parents in child health care settings.

Key words: thirdhand smoke; smoking; tobacco; indoor air quality; smoking cessation; pediatrics.

 

While “thirdhand smoke” may be a relatively new term, it is rooted in an old concept—the particulate matter and residue from tobacco smoke left behind after tobacco is burned. In 1953, Dr. Ernest Wynder and his colleagues from the Washington University School of Medicine in St. Louis showed that condensate made from the residue of cigarette smoke causes cancer [1]. This residue left behind by burning cigarettes is now known as thirdhand smoke [2]. Dr. Wynder used acetone to rinse the leftover tobacco smoke residue from a smoking chamber where he had burned cigarettes. He then painted the solution of acetone and thirdhand smoke residue onto the backs of mice. The results of Dr. Wynder’s study demonstrated that exposed mice developed cancerous skin lesions, whereas mice exposed to the acetone alone did not display skin lesions. Dr. Wynder sounded an alarm bell in his manuscript when he wrote, “Such studies, in view of the corollary clinical data relating smoking to various types of cancer, appear urgent. They may result not only in furthering our knowledge of carcinogenesis, but in promoting some practical aspects of cancer prevention [1].”

Decades of research has been conducted since Dr. Wynder’s discovery to definitively conclude that smoking tobacco and exposure to secondhand tobacco smoke is harmful to human health. It is estimated that 480,000 annual premature deaths in the United States alone are attributable to smoking and exposure to secondhand smoke [3]. The World Health Organization estimates that worldwide tobacco use is responsible for more than 7 million deaths per year, with 890,000 of those deaths caused by secondhand smoke exposure of nonsmokers [4]. Epidemiological evidence of the harm posed by tobacco has spurred the U.S Surgeon General to conclude that there is no risk-free level of exposure to tobacco smoke [5]. Despite the overwhelming evidence implicating tobacco as the cause of an unprecedented amount of disease resulting from the use of a consumer product, only recently has a dedicated research agenda been pursued to study what Dr. Wynder urgently called for back in 1953: further exploration of the health effects of thirdhand tobacco smoke.

The term "thirdhand smoke" was first coined in 2006 by researchers with the Clinical Effort Against Secondhand Smoke Exposure (CEASE) program at Massachusetts General Hospital in Boston [6], and recent research has begun to shed considerable light on the topic. In 2011, a research consortium of scientists funded by the Tobacco-Related Disease Research Program [7] in California was set up to conduct pioneering research on the characterization, exposure and health effects of thirdhand tobacco smoke [8]. Research findings from this consortium and other scientists from around the world are quickly expanding and disseminating knowledge on this important topic.

While the research on thirdhand smoke is ongoing, this paper summarizes the current literature most relevant to the pediatric population and outlines clinical and policy recommendations to protect children and families from the harms of exposure to thirdhand smoke.

What Is Thirdhand Smoke and How Is It Different from Secondhand Smoke?

Thirdhand smoke is a result of combusted tobacco, most often from smoking cigarettes, pipes, cigars, or cigarillos. Thirdhand smoke remains on surfaces and in dust for a longtime after smoking happens, reacts with oxidants and other compounds to form secondary pollutants, and is re-emitted as a gas and/or resuspended when particles are disturbed and go back into the air where they can be inhaled [9]. One dramatic example of how thirdhand smoke can remain on surfaces long after secondhand smoke dissipates was discovered on the ornate constellation ceiling in the main concourse of the Grand Central Terminal in New York City. According to Sam Roberts, a correspondent for the New York Times and the author of a book about the historic train station, the dark residue that accumulated on the concourse ceiling over decades and was originally believed to be the result of soot from train engines was primarily residue from tobacco smoke [10–12]. It wasn’t until a restoration in the 1990s when workers scrubbed the tar and nicotine residue from the ceiling could the elaborate design of the zodiac signs and constellations be seen again [13]. A similar process takes place inside homes, where smoke residue accumulates on surfaces such as walls and ceilings after smoking happens. Owners of homes that have been previously smoked in are faced with unanswered questions about how to clean up the toxic substances left behind.

When tobacco is smoked, the particulates contained in secondhand smoke settle on surfaces; this contamination is absorbed deep into materials such as hair, clothes, carpeting, furniture, and wallboard [9,14]. After depositing onto surfaces, the chemicals undergo an aging process, which changes the chemical structure of the smoke pollutants. The nicotine in thirdhand smoke residue reacts with common indoor air pollutants, such as nitrous acid and ozone, to form hazardous substances. When the nicotine present in thirdhand smoke reacts with nitrous acid, it forms carcinogenic tobacco-specific nitrosamines such as NNK and NNN [15–17]. Nicotine also reacts with ozone to form additional harmful ultrafine particles that can embed deep within the lungs when inhaled [18]. As thirdhand smoke ages, it becomes more toxic [15]. The aged particles then undergo a process called “off-gassing,” in which gas is continuously re-emitted from these surfaces back into the air [19]. This process of off-gassing occurs long after cigarettes have been smoked indoors [19,20]. Thirdhand smoke particles can also be inhaled when they get resuspended into the air after contaminated surfaces are disturbed [21].

Common practices employed by smokers, like smoking in different rooms, using fans to diffuse the smoke, or opening windows, do not prevent the formation and inhalation of thirdhand smoke by people living or visiting these indoor spaces [22]. Environments with potential thirdhand smoke exposure include homes of smokers [23], apartments and homes previously occupied by smokers [24], multiunit housing where smoking is permitted [25], automobiles that have been smoked in [26], hotel rooms where smoking is permitted [27], and other indoor places where smoking has occurred.

Research Supports Having Completely Smoke-Free Environments

Recent research has shown that exposure to thirdhand smoke is harmful. These findings, many of which are described below, offer strong support in favor of advocating for environments free of thirdhand smoke contamination for families and children.

Genetic Damage from Thirdhand Smoke Exposure

In 2013, researchers from the Lawrence Berkeley National Laboratory were the first to demonstrate that thirdhand smoke causes significant genetic damage to human cells [28]. Using in vitro assays, the researchers showed that thirdhand smoke is a cause of harm to human DNA in the form of strand breaks and oxidative damage, which leads to mutations that can cause cancer. The researches also specifically tested the effect of NNA, a tobacco-specific nitrosamine that is commonly found in thirdhand smoke but not in secondhand smoke, on human cell cultures and found that it caused significant damage to DNA [28].

Children Show Elevated Biomarkers of Thirdhand Smoke Exposure in Their Urine and Hair Samples

In 2004, Matt and colleagues described how they collected household dust samples from living rooms and infants’ bedrooms [23]. Their research demonstrated that nicotine accumulated on the living room and infants’ bedroom surfaces of the homes belonging to smokers. Significantly higher amounts of urine cotinine, a biomarker for exposure to nicotine, were detected among infants who lived in homes where smoking happens inside compared to homes where smokers go outside to smoke [23]. As well, a study published in 2017 that measured the presence of hand nicotine on children of smokers who presented to the emergency room for an illness possibly related to tobacco smoke exposure detected hand nicotine on the hands of each child who participated in this pilot study. The researchers found a positive correlation between the amount of nicotine found on children’s hands and the amount of cotinine, a biomarker for nicotine exposure, detected in the children’s saliva [29].

Children Are Exposed to Higher Ratios of Thirdhand Smoke than Adults

In 2009, researchers discovered that the thirdhand smoke ratio of tobacco-specific nitrosamines to nicotine increases during the aging process [9]. Biomarkers measured in the urine can now be used to estimate the degree to which people have been exposed to secondhand or thirdhand smoke based on the ratio of the thirdhand smoke biomarker NNK and nicotine. Toddlers who live with adults who smoke have higher NNK/nicotine ratios, suggesting that they are exposed to a higher ratio of thirdhand smoke compared to secondhand smoke than adults [30]. Young children are likely exposed to higher ratios of thirdhand smoke as they spend more time on the floor, where thirdhand smoke accumulates. They frequently put their hands and other objects into their mouths. Young children breathe faster than adults, increasing their inhalation exposure and also have thinner skin, making dermal absorption more efficient [9].

Modeling Excess Cancer Risk

A 2014 United Kingdom study used official sources of toxicological data about chemicals detected in thirdhand smoke–contaminated homes to assess excess cancer risk posed from thirdhand smoke [17]. Using dust samples collected from homes where a smoker lived, they estimate that the median lifetime excess cancer risk from the exposure to all the nitrosamines present in thirdhand smoke is 9.6 additional cancer cases per 100,000 children exposed and could be as high as 1 excess cancer case per 1000 children exposed. The researchers concluded that young children aged 1 to 6 are at an especially increased risk for cancer because of their frequent contact with surfaces contaminated with thirdhand smoke and their ingestion of the particulate matter that settles on surfaces after smoking takes place [17].

 

 

Infants in Health Care Facilities Are Exposed to Thirdhand Smoke

Researchers have observed biomarkers confirming thirdhand smoke exposure in the urine of infants in the NICU. Found in incubators and cribs, particulates are likely being deposited in the NICU from visitors who have thirdhand smoke on their clothing, skin, and hair [31].

Animal Studies Link Thirdhand Smoke Exposure to Common Human Disease

Mice exposed to thirdhand smoke under conditions meant to simulate levels similar to human exposure are pre-diabetic, are at higher risk of developing metabolic syndrome, have inflammatory markers in the lungs that increase the risk for asthma, show slow wound healing, develop nonalcoholic fatty liver disease, and become behaviorally hyperactive [32]. Another recent study published in 2017 showed that mice exposed to thirdhand smoke after birth weighed less than mice not exposed to thirdhand smoke. Additionally, mice exposed to thirdhand smoke early in life showed changes in white blood cell counts that persisted into adulthood [9,33].

Summary

In summary, recent research makes a compelling case for invoking the precautionary principle to ensure that children avoid exposures to thirdhand smoke in their homes, cars, and healthcare settings. Studies reveal that:

  • children live in homes where thirdhand smoke is present and this exposure is detectable in their bodies [23]
  • concentrations of thirdhand smoke exposure observed in children are disproportionately higher than adults [30]
  • chemicals present in thirdhand smoke cause damage to DNA [28]
  • thirdhand smoke contains carcinogens that put exposed children at increased risk of cancer [17]
  • thirdhand smoke is being detected within medical settings [34] and in the bodies of medically-vulnerable children [29], and
  • animal studies have linked exposure to thirdhand smoke to a number of adverse health conditions commonly seen in today’s pediatric population such as metabolic syndrome, prediabetes, asthma, hyperactivity [32] and low birth weight [33].

Using the Thirdhand Smoke Concept in Clinical Practice

The clinical setting is an ideal place to address thirdhand smoke with families as a component of a comprehensive tobacco control strategy.

The Cessation Imperative—A Novel Motivational Message Prompted by Thirdhand Smoke

While there are potentially many ways to address thirdhand smoke exposure with families, the CEASE program has been used in the primary care setting to train child health care clinicians and office staff to address second- and thirdhand smoke. The training also educates clinicians on providing cessation counseling and resources to families with the goal of helping all family members become tobacco free, as well as to helping families keep completely smoke-free homes and cars [35,36]. The concept of thirdhand smoke creates what we have coined the cessation imperative [36]. The cessation imperative is based on the notion that the only way to protect non-smoking family and household members from thirdhand smoke is for all household smokers to quit smoking completely. Smoking, even when not in the presence of children, can expose others to toxic contaminates that settle on the surfaces of the home, the car as well as to the skin, hair, and clothing of family members who smoke. A discussion with parents about eliminating only secondhand smoke exposure for children does not adequately address how continued smoking, even when children are not present, can be harmful. The thirdhand smoke concept can be presented early, making it an efficient way to advocate for completely smoke-free families.

Thirdhand Smoke Counseling Helps Clinicians Achieve Key Tobacco Control Goals

The American Academy of Pediatrics (AAP) and the American Academy of Family Physicians (AAFP) recommend that health care providers deliver advice to parents regarding establishing smoke-free homes and cars and provide information about how their smoking adversely affects their children’s health [37,38]. It is AAP and AAFP policy that health care providers provide tobacco dependence treatment and referral to cessation services to help adult family members quit smoking [38,39]. Successfully integrating counseling around the topic of thirdhand smoke into existing smoking cessation service delivery is possible. The CEASE research and implementation team developed and disseminated educational content to clinicians about thirdhand smoke through AAP courses delivered online [40] as well as made presentations to clinicians at AAP-sponsored training sessions. Thirdhand smoke messaging has been included in the CEASE practice trainings so that participating clinicians in pediatric offices are equipped to engage parents on this topic. Further information about these educational resources and opportunities can be obtained from the AAP Julius B. Richmond Center of Excellence website [41] and from the Massachusetts General Hospital CEASE program’s website [42].

Counseling parents about thirdhand smoke can help assist parents with their smoking in the critical context of their child’s care. Most parents see their child’s health care clinician more often than their own [43]. Increasing the number of pediatric clinical encounters where parental smoking is addressed while also increasing the effectiveness of these clinical encounters by increasing parents’ motivation to protect their children from tobacco smoke exposure are important goals. The topic of thirdhand smoke is a novel concept that clinicians can use to engage with parents around their smoking in a new way. Recent research conducted by the CEASE team suggests that counseling parents in the pediatric setting about thirdhand smoke can be useful in helping achieve tobacco control goals with families. Parent’s belief about thirdhand smoke is associated with the likelihood the parent will take concrete steps to protect their child. Parents who believe thirdhand smoke is harmful are more likely to protect their children from exposure by adopting strictly enforced smoke-free home and car rules [44]. Parents who changed their thirdhand smoke beliefs over the course of a year to believing that thirdhand smoke is harmful were more likely to try to quit smoking [44].

Child health care clinicians are effective at influencing parents’ beliefs about the potential harm thirdhand smoke poses to their children. Parents who received advice from pediatricians to quit smoking or to adopt smoke-free home or policies were more likely to believe that thirdhand smoke was harmful to the health of children [45]. Fathers (as compared with mothers) and parents who smoked more cigarettes each day were less likely to accept that thirdhand smoke is harmful to children [45]. Conversely, delivering effective educational messages and counseling around the topic of thirdhand smoke to parents may help promote smoke-free rules and acceptance of cessation assistance.

 

 

Protect Patients from Thirdhand Smoke Risks

All health care settings should be completely smoke-free. Smoking bans help protect all families and children from second and thirdhand smoke exposure. It is especially important for medically vulnerable children to visit facilities free from all forms of tobacco smoke contamination. CEASE trainings encourage practices to implement a zone of wellness on the grounds of the healthcare facility by completely banning smoking. The CEASE implementation team also trains practice leaders to reach out to all staff that use tobacco and offer resources and support for quitting. Having a non-smoking staff sets a great example for families who visit the healthcare facility, and reduces the likelihood of bringing thirdhand smoke contaminates into the facility. Creating a policy that addresses thirdhand smoke exposure is a concrete step that health care organizations can take to protect patients.

Thirdhand Smoke Resources Developed and/or Used by the CEASE Program

The CEASE program has developed and/or identified a number of clinical resources to educate parents and clinicians about thirdhand smoke. These free resources can enhance awareness of thirdhand smoke and help promote the use of the thirdhand smoke concept in clinical practice.

  • Posters with messages designed to educate parents about thirdhand smoke to encourage receipt of cessation resources were created for use in waiting areas and exam rooms of child health care practices. A poster for clinical practice (Figure 1) can be downloaded and printed from the CEASE program website [42].
  • Health education handouts that directly address thirdhand smoke exposure are available. The handouts can be taken home to family members who are not present at the visit and contain the telephone number for the tobacco quitline service, which connects smokers in the United States with free telephone support for smoking cessation. Handouts for clinical practice can be downloaded and printed from the CEASE program website. Figure 2 shows a handout that encourages parents to keep a smoke-free car by pointing out that tobacco smoke stays in the car long after the cigarette is out.
  • Videos about thirdhand smoke can be viewed by parents while in child health care offices or shared on practice websites or social media platforms. The CEASE program encourages practices to distribute videos about thirdhand smoke to introduce parents to the concept of thirdhand smoke and to encourage parents to engage in a discussion with their child’s clinicians about ways to limit thirdhand smoke exposure. Suitable videos for parental viewing include the 2 listed below, which highlight information from the Thirdhand Smoke Research Consortium.
      -University of California Riverside https://youtu.be/i1rhqRy-2e8
     -San Diego State University https://youtu.be/rqzi-9sXLdU
  • Letters for landlords and management companies were created to stress the importance of providing a smoke-free living environment for children. The letters are meant to be signed by the child’s health care provider. The letters state that eliminating smoking in their buildings would result in landlords that “Pay less for cleaning and turnover fees.” Landlord letter templates can be downloaded and printed from the CEASE program website [42].
  • Educational content for child health care clinicians about thirdhand smoke and how to counsel parents is included in the American Academy of Pediatrics Education in Quality Improvement for Pediatric Practice (EQIPP) online course entitled “Eliminating Tobacco” Use and Exposure to Secondhand Smoke. A section devoted to educating clinicians on the topic of thirdhand smoke is presented in this course. The course can be accessed through the AAP website and it qualifies for American Board of Pediatrics maintenance of certification part IV credit [40].

The CEASE team has worked with mass media outlets to communicate the messages about thirdhand smoke to build public awareness. The Today Show helped to popularize the concept of thirdhand smoke in 2009 after a paper published in the journal Pediatrics linked thirdhand smoke beliefs to home smoking bans [2].

 

 

Systems Approaches to Reduce Thirdhand Smoke Exposure

Public Policy Approaches

A clear policy agenda can help people protect their families from exposure to thirdhand smoke [46]. Policy approaches that have worked for lead, asbestos, and radon are examples of common household contaminants that are regulated using different mechanisms in an effort to protect the public health [46]. Strengths and weaknesses in each of these different approaches should be carefully considered when developing a comprehensive policy agenda to address thirdhand smoke. Recently, research on the health effects of thirdhand smoke spurred the passage of California legislative bill AB 1819 that “prohibits smoking tobacco at all times in the homes of licensed family child care homes and in areas where children are present [47].” As well, a recent US Department of Housing and Urban Development rule was finalized that requires all public housing agencies to implement a smoke-free policy by 30 July 2018 [48]. Smoke-free housing protects occupants from both secondhand and thirdhand smoke exposure. Pediatricians and other child health care professionals are well positioned to advocate for legislative actions that protect children from harmful exposures to thirdhand smoke.

Practice Change in Child Health Care Settings

Designing health care systems to screen for tobacco smoke exposure and to provide evidence-based cessation resources for all smokers is one of the best ways to reduce exposures to thirdhand smoke. Preventing thirdhand smoke exposure can work as novel messaging to promote tobacco cessation programs. Developing electronic medical record systems that allow for documentation of the smoking status of household members and whether or not homes and cars are completely smokefree can be particularly helpful tools for child health care providers when addressing thirdhand smoke with families. Good documentation about smoke-free homes and cars can enhance follow-up discussions with families as they work towards reducing thirdhand smoke exposures.

Summary

The thirdhand smoke concept has been used to improve delivery of tobacco control counseling and services for parents in the child health care context. Free materials are available that utilize thirdhand smoke messaging. As the science of thirdhand smoke matures, it will increasingly be used to help promote completely smoke-free places. The existing research on thirdhand smoke establishes the need for clinicians to communicate the cessation imperative. By using it, clinicians can help all smokers and non-smokers understand that there is no way to smoke tobacco without exposing friends and family.

 

Corresponding author: Jeremy E. Drehmer, MPH, 125 Nashua St., Suite 860, Boston, MA 02114, jdrehmer@ mgh.harvard.edu.

Financial disclosures: None

From the Center for Child and Adolescent Health Research and Policy, Division of General Academic Pediatrics, Massachusetts General Hospital for Children, and the Tobacco Research and Treatment Center, Massachusetts General Hospital, Boston, MA.

 

Abstract

  • Objective: To explain the concept of thirdhand smoke and how it can be used to protect the health of children and improve delivery of tobacco control interventions for parents in the child health care setting.
  • Methods: Review of the literature and descriptive report.
  • Results: The thirdhand smoke concept has been used in the CEASE intervention to improve the delivery of tobacco control counseling and services to parents. Materials and techniques have been developed for the child health care setting that use the concept of thirdhand smoke. Scientific findings demonstrate that thirdhand smoke exposure is harmful and establishes the need for clinicians to communicate the cessation imperative: the only way to protect non-smoking household members from thirdhand smoke is for all household smokers to quit smoking completely. As the scientific knowledge of thirdhand smoke increases, advocates will likely rely on it to encourage completely smoke-free places.
  • Conclusion: Recent scientific studies on thirdhand smoke are impelling further research on the topic, spurring the creation of tobacco control policies to protect people from thridhand smoke and stimulating improvements to the delivery of tobacco control counseling and services to parents in child health care settings.

Key words: thirdhand smoke; smoking; tobacco; indoor air quality; smoking cessation; pediatrics.

 

While “thirdhand smoke” may be a relatively new term, it is rooted in an old concept—the particulate matter and residue from tobacco smoke left behind after tobacco is burned. In 1953, Dr. Ernest Wynder and his colleagues from the Washington University School of Medicine in St. Louis showed that condensate made from the residue of cigarette smoke causes cancer [1]. This residue left behind by burning cigarettes is now known as thirdhand smoke [2]. Dr. Wynder used acetone to rinse the leftover tobacco smoke residue from a smoking chamber where he had burned cigarettes. He then painted the solution of acetone and thirdhand smoke residue onto the backs of mice. The results of Dr. Wynder’s study demonstrated that exposed mice developed cancerous skin lesions, whereas mice exposed to the acetone alone did not display skin lesions. Dr. Wynder sounded an alarm bell in his manuscript when he wrote, “Such studies, in view of the corollary clinical data relating smoking to various types of cancer, appear urgent. They may result not only in furthering our knowledge of carcinogenesis, but in promoting some practical aspects of cancer prevention [1].”

Decades of research has been conducted since Dr. Wynder’s discovery to definitively conclude that smoking tobacco and exposure to secondhand tobacco smoke is harmful to human health. It is estimated that 480,000 annual premature deaths in the United States alone are attributable to smoking and exposure to secondhand smoke [3]. The World Health Organization estimates that worldwide tobacco use is responsible for more than 7 million deaths per year, with 890,000 of those deaths caused by secondhand smoke exposure of nonsmokers [4]. Epidemiological evidence of the harm posed by tobacco has spurred the U.S Surgeon General to conclude that there is no risk-free level of exposure to tobacco smoke [5]. Despite the overwhelming evidence implicating tobacco as the cause of an unprecedented amount of disease resulting from the use of a consumer product, only recently has a dedicated research agenda been pursued to study what Dr. Wynder urgently called for back in 1953: further exploration of the health effects of thirdhand tobacco smoke.

The term "thirdhand smoke" was first coined in 2006 by researchers with the Clinical Effort Against Secondhand Smoke Exposure (CEASE) program at Massachusetts General Hospital in Boston [6], and recent research has begun to shed considerable light on the topic. In 2011, a research consortium of scientists funded by the Tobacco-Related Disease Research Program [7] in California was set up to conduct pioneering research on the characterization, exposure and health effects of thirdhand tobacco smoke [8]. Research findings from this consortium and other scientists from around the world are quickly expanding and disseminating knowledge on this important topic.

While the research on thirdhand smoke is ongoing, this paper summarizes the current literature most relevant to the pediatric population and outlines clinical and policy recommendations to protect children and families from the harms of exposure to thirdhand smoke.

What Is Thirdhand Smoke and How Is It Different from Secondhand Smoke?

Thirdhand smoke is a result of combusted tobacco, most often from smoking cigarettes, pipes, cigars, or cigarillos. Thirdhand smoke remains on surfaces and in dust for a longtime after smoking happens, reacts with oxidants and other compounds to form secondary pollutants, and is re-emitted as a gas and/or resuspended when particles are disturbed and go back into the air where they can be inhaled [9]. One dramatic example of how thirdhand smoke can remain on surfaces long after secondhand smoke dissipates was discovered on the ornate constellation ceiling in the main concourse of the Grand Central Terminal in New York City. According to Sam Roberts, a correspondent for the New York Times and the author of a book about the historic train station, the dark residue that accumulated on the concourse ceiling over decades and was originally believed to be the result of soot from train engines was primarily residue from tobacco smoke [10–12]. It wasn’t until a restoration in the 1990s when workers scrubbed the tar and nicotine residue from the ceiling could the elaborate design of the zodiac signs and constellations be seen again [13]. A similar process takes place inside homes, where smoke residue accumulates on surfaces such as walls and ceilings after smoking happens. Owners of homes that have been previously smoked in are faced with unanswered questions about how to clean up the toxic substances left behind.

When tobacco is smoked, the particulates contained in secondhand smoke settle on surfaces; this contamination is absorbed deep into materials such as hair, clothes, carpeting, furniture, and wallboard [9,14]. After depositing onto surfaces, the chemicals undergo an aging process, which changes the chemical structure of the smoke pollutants. The nicotine in thirdhand smoke residue reacts with common indoor air pollutants, such as nitrous acid and ozone, to form hazardous substances. When the nicotine present in thirdhand smoke reacts with nitrous acid, it forms carcinogenic tobacco-specific nitrosamines such as NNK and NNN [15–17]. Nicotine also reacts with ozone to form additional harmful ultrafine particles that can embed deep within the lungs when inhaled [18]. As thirdhand smoke ages, it becomes more toxic [15]. The aged particles then undergo a process called “off-gassing,” in which gas is continuously re-emitted from these surfaces back into the air [19]. This process of off-gassing occurs long after cigarettes have been smoked indoors [19,20]. Thirdhand smoke particles can also be inhaled when they get resuspended into the air after contaminated surfaces are disturbed [21].

Common practices employed by smokers, like smoking in different rooms, using fans to diffuse the smoke, or opening windows, do not prevent the formation and inhalation of thirdhand smoke by people living or visiting these indoor spaces [22]. Environments with potential thirdhand smoke exposure include homes of smokers [23], apartments and homes previously occupied by smokers [24], multiunit housing where smoking is permitted [25], automobiles that have been smoked in [26], hotel rooms where smoking is permitted [27], and other indoor places where smoking has occurred.

Research Supports Having Completely Smoke-Free Environments

Recent research has shown that exposure to thirdhand smoke is harmful. These findings, many of which are described below, offer strong support in favor of advocating for environments free of thirdhand smoke contamination for families and children.

Genetic Damage from Thirdhand Smoke Exposure

In 2013, researchers from the Lawrence Berkeley National Laboratory were the first to demonstrate that thirdhand smoke causes significant genetic damage to human cells [28]. Using in vitro assays, the researchers showed that thirdhand smoke is a cause of harm to human DNA in the form of strand breaks and oxidative damage, which leads to mutations that can cause cancer. The researches also specifically tested the effect of NNA, a tobacco-specific nitrosamine that is commonly found in thirdhand smoke but not in secondhand smoke, on human cell cultures and found that it caused significant damage to DNA [28].

Children Show Elevated Biomarkers of Thirdhand Smoke Exposure in Their Urine and Hair Samples

In 2004, Matt and colleagues described how they collected household dust samples from living rooms and infants’ bedrooms [23]. Their research demonstrated that nicotine accumulated on the living room and infants’ bedroom surfaces of the homes belonging to smokers. Significantly higher amounts of urine cotinine, a biomarker for exposure to nicotine, were detected among infants who lived in homes where smoking happens inside compared to homes where smokers go outside to smoke [23]. As well, a study published in 2017 that measured the presence of hand nicotine on children of smokers who presented to the emergency room for an illness possibly related to tobacco smoke exposure detected hand nicotine on the hands of each child who participated in this pilot study. The researchers found a positive correlation between the amount of nicotine found on children’s hands and the amount of cotinine, a biomarker for nicotine exposure, detected in the children’s saliva [29].

Children Are Exposed to Higher Ratios of Thirdhand Smoke than Adults

In 2009, researchers discovered that the thirdhand smoke ratio of tobacco-specific nitrosamines to nicotine increases during the aging process [9]. Biomarkers measured in the urine can now be used to estimate the degree to which people have been exposed to secondhand or thirdhand smoke based on the ratio of the thirdhand smoke biomarker NNK and nicotine. Toddlers who live with adults who smoke have higher NNK/nicotine ratios, suggesting that they are exposed to a higher ratio of thirdhand smoke compared to secondhand smoke than adults [30]. Young children are likely exposed to higher ratios of thirdhand smoke as they spend more time on the floor, where thirdhand smoke accumulates. They frequently put their hands and other objects into their mouths. Young children breathe faster than adults, increasing their inhalation exposure and also have thinner skin, making dermal absorption more efficient [9].

Modeling Excess Cancer Risk

A 2014 United Kingdom study used official sources of toxicological data about chemicals detected in thirdhand smoke–contaminated homes to assess excess cancer risk posed from thirdhand smoke [17]. Using dust samples collected from homes where a smoker lived, they estimate that the median lifetime excess cancer risk from the exposure to all the nitrosamines present in thirdhand smoke is 9.6 additional cancer cases per 100,000 children exposed and could be as high as 1 excess cancer case per 1000 children exposed. The researchers concluded that young children aged 1 to 6 are at an especially increased risk for cancer because of their frequent contact with surfaces contaminated with thirdhand smoke and their ingestion of the particulate matter that settles on surfaces after smoking takes place [17].

 

 

Infants in Health Care Facilities Are Exposed to Thirdhand Smoke

Researchers have observed biomarkers confirming thirdhand smoke exposure in the urine of infants in the NICU. Found in incubators and cribs, particulates are likely being deposited in the NICU from visitors who have thirdhand smoke on their clothing, skin, and hair [31].

Animal Studies Link Thirdhand Smoke Exposure to Common Human Disease

Mice exposed to thirdhand smoke under conditions meant to simulate levels similar to human exposure are pre-diabetic, are at higher risk of developing metabolic syndrome, have inflammatory markers in the lungs that increase the risk for asthma, show slow wound healing, develop nonalcoholic fatty liver disease, and become behaviorally hyperactive [32]. Another recent study published in 2017 showed that mice exposed to thirdhand smoke after birth weighed less than mice not exposed to thirdhand smoke. Additionally, mice exposed to thirdhand smoke early in life showed changes in white blood cell counts that persisted into adulthood [9,33].

Summary

In summary, recent research makes a compelling case for invoking the precautionary principle to ensure that children avoid exposures to thirdhand smoke in their homes, cars, and healthcare settings. Studies reveal that:

  • children live in homes where thirdhand smoke is present and this exposure is detectable in their bodies [23]
  • concentrations of thirdhand smoke exposure observed in children are disproportionately higher than adults [30]
  • chemicals present in thirdhand smoke cause damage to DNA [28]
  • thirdhand smoke contains carcinogens that put exposed children at increased risk of cancer [17]
  • thirdhand smoke is being detected within medical settings [34] and in the bodies of medically-vulnerable children [29], and
  • animal studies have linked exposure to thirdhand smoke to a number of adverse health conditions commonly seen in today’s pediatric population such as metabolic syndrome, prediabetes, asthma, hyperactivity [32] and low birth weight [33].

Using the Thirdhand Smoke Concept in Clinical Practice

The clinical setting is an ideal place to address thirdhand smoke with families as a component of a comprehensive tobacco control strategy.

The Cessation Imperative—A Novel Motivational Message Prompted by Thirdhand Smoke

While there are potentially many ways to address thirdhand smoke exposure with families, the CEASE program has been used in the primary care setting to train child health care clinicians and office staff to address second- and thirdhand smoke. The training also educates clinicians on providing cessation counseling and resources to families with the goal of helping all family members become tobacco free, as well as to helping families keep completely smoke-free homes and cars [35,36]. The concept of thirdhand smoke creates what we have coined the cessation imperative [36]. The cessation imperative is based on the notion that the only way to protect non-smoking family and household members from thirdhand smoke is for all household smokers to quit smoking completely. Smoking, even when not in the presence of children, can expose others to toxic contaminates that settle on the surfaces of the home, the car as well as to the skin, hair, and clothing of family members who smoke. A discussion with parents about eliminating only secondhand smoke exposure for children does not adequately address how continued smoking, even when children are not present, can be harmful. The thirdhand smoke concept can be presented early, making it an efficient way to advocate for completely smoke-free families.

Thirdhand Smoke Counseling Helps Clinicians Achieve Key Tobacco Control Goals

The American Academy of Pediatrics (AAP) and the American Academy of Family Physicians (AAFP) recommend that health care providers deliver advice to parents regarding establishing smoke-free homes and cars and provide information about how their smoking adversely affects their children’s health [37,38]. It is AAP and AAFP policy that health care providers provide tobacco dependence treatment and referral to cessation services to help adult family members quit smoking [38,39]. Successfully integrating counseling around the topic of thirdhand smoke into existing smoking cessation service delivery is possible. The CEASE research and implementation team developed and disseminated educational content to clinicians about thirdhand smoke through AAP courses delivered online [40] as well as made presentations to clinicians at AAP-sponsored training sessions. Thirdhand smoke messaging has been included in the CEASE practice trainings so that participating clinicians in pediatric offices are equipped to engage parents on this topic. Further information about these educational resources and opportunities can be obtained from the AAP Julius B. Richmond Center of Excellence website [41] and from the Massachusetts General Hospital CEASE program’s website [42].

Counseling parents about thirdhand smoke can help assist parents with their smoking in the critical context of their child’s care. Most parents see their child’s health care clinician more often than their own [43]. Increasing the number of pediatric clinical encounters where parental smoking is addressed while also increasing the effectiveness of these clinical encounters by increasing parents’ motivation to protect their children from tobacco smoke exposure are important goals. The topic of thirdhand smoke is a novel concept that clinicians can use to engage with parents around their smoking in a new way. Recent research conducted by the CEASE team suggests that counseling parents in the pediatric setting about thirdhand smoke can be useful in helping achieve tobacco control goals with families. Parent’s belief about thirdhand smoke is associated with the likelihood the parent will take concrete steps to protect their child. Parents who believe thirdhand smoke is harmful are more likely to protect their children from exposure by adopting strictly enforced smoke-free home and car rules [44]. Parents who changed their thirdhand smoke beliefs over the course of a year to believing that thirdhand smoke is harmful were more likely to try to quit smoking [44].

Child health care clinicians are effective at influencing parents’ beliefs about the potential harm thirdhand smoke poses to their children. Parents who received advice from pediatricians to quit smoking or to adopt smoke-free home or policies were more likely to believe that thirdhand smoke was harmful to the health of children [45]. Fathers (as compared with mothers) and parents who smoked more cigarettes each day were less likely to accept that thirdhand smoke is harmful to children [45]. Conversely, delivering effective educational messages and counseling around the topic of thirdhand smoke to parents may help promote smoke-free rules and acceptance of cessation assistance.

 

 

Protect Patients from Thirdhand Smoke Risks

All health care settings should be completely smoke-free. Smoking bans help protect all families and children from second and thirdhand smoke exposure. It is especially important for medically vulnerable children to visit facilities free from all forms of tobacco smoke contamination. CEASE trainings encourage practices to implement a zone of wellness on the grounds of the healthcare facility by completely banning smoking. The CEASE implementation team also trains practice leaders to reach out to all staff that use tobacco and offer resources and support for quitting. Having a non-smoking staff sets a great example for families who visit the healthcare facility, and reduces the likelihood of bringing thirdhand smoke contaminates into the facility. Creating a policy that addresses thirdhand smoke exposure is a concrete step that health care organizations can take to protect patients.

Thirdhand Smoke Resources Developed and/or Used by the CEASE Program

The CEASE program has developed and/or identified a number of clinical resources to educate parents and clinicians about thirdhand smoke. These free resources can enhance awareness of thirdhand smoke and help promote the use of the thirdhand smoke concept in clinical practice.

  • Posters with messages designed to educate parents about thirdhand smoke to encourage receipt of cessation resources were created for use in waiting areas and exam rooms of child health care practices. A poster for clinical practice (Figure 1) can be downloaded and printed from the CEASE program website [42].
  • Health education handouts that directly address thirdhand smoke exposure are available. The handouts can be taken home to family members who are not present at the visit and contain the telephone number for the tobacco quitline service, which connects smokers in the United States with free telephone support for smoking cessation. Handouts for clinical practice can be downloaded and printed from the CEASE program website. Figure 2 shows a handout that encourages parents to keep a smoke-free car by pointing out that tobacco smoke stays in the car long after the cigarette is out.
  • Videos about thirdhand smoke can be viewed by parents while in child health care offices or shared on practice websites or social media platforms. The CEASE program encourages practices to distribute videos about thirdhand smoke to introduce parents to the concept of thirdhand smoke and to encourage parents to engage in a discussion with their child’s clinicians about ways to limit thirdhand smoke exposure. Suitable videos for parental viewing include the 2 listed below, which highlight information from the Thirdhand Smoke Research Consortium.
      -University of California Riverside https://youtu.be/i1rhqRy-2e8
     -San Diego State University https://youtu.be/rqzi-9sXLdU
  • Letters for landlords and management companies were created to stress the importance of providing a smoke-free living environment for children. The letters are meant to be signed by the child’s health care provider. The letters state that eliminating smoking in their buildings would result in landlords that “Pay less for cleaning and turnover fees.” Landlord letter templates can be downloaded and printed from the CEASE program website [42].
  • Educational content for child health care clinicians about thirdhand smoke and how to counsel parents is included in the American Academy of Pediatrics Education in Quality Improvement for Pediatric Practice (EQIPP) online course entitled “Eliminating Tobacco” Use and Exposure to Secondhand Smoke. A section devoted to educating clinicians on the topic of thirdhand smoke is presented in this course. The course can be accessed through the AAP website and it qualifies for American Board of Pediatrics maintenance of certification part IV credit [40].

The CEASE team has worked with mass media outlets to communicate the messages about thirdhand smoke to build public awareness. The Today Show helped to popularize the concept of thirdhand smoke in 2009 after a paper published in the journal Pediatrics linked thirdhand smoke beliefs to home smoking bans [2].

 

 

Systems Approaches to Reduce Thirdhand Smoke Exposure

Public Policy Approaches

A clear policy agenda can help people protect their families from exposure to thirdhand smoke [46]. Policy approaches that have worked for lead, asbestos, and radon are examples of common household contaminants that are regulated using different mechanisms in an effort to protect the public health [46]. Strengths and weaknesses in each of these different approaches should be carefully considered when developing a comprehensive policy agenda to address thirdhand smoke. Recently, research on the health effects of thirdhand smoke spurred the passage of California legislative bill AB 1819 that “prohibits smoking tobacco at all times in the homes of licensed family child care homes and in areas where children are present [47].” As well, a recent US Department of Housing and Urban Development rule was finalized that requires all public housing agencies to implement a smoke-free policy by 30 July 2018 [48]. Smoke-free housing protects occupants from both secondhand and thirdhand smoke exposure. Pediatricians and other child health care professionals are well positioned to advocate for legislative actions that protect children from harmful exposures to thirdhand smoke.

Practice Change in Child Health Care Settings

Designing health care systems to screen for tobacco smoke exposure and to provide evidence-based cessation resources for all smokers is one of the best ways to reduce exposures to thirdhand smoke. Preventing thirdhand smoke exposure can work as novel messaging to promote tobacco cessation programs. Developing electronic medical record systems that allow for documentation of the smoking status of household members and whether or not homes and cars are completely smokefree can be particularly helpful tools for child health care providers when addressing thirdhand smoke with families. Good documentation about smoke-free homes and cars can enhance follow-up discussions with families as they work towards reducing thirdhand smoke exposures.

Summary

The thirdhand smoke concept has been used to improve delivery of tobacco control counseling and services for parents in the child health care context. Free materials are available that utilize thirdhand smoke messaging. As the science of thirdhand smoke matures, it will increasingly be used to help promote completely smoke-free places. The existing research on thirdhand smoke establishes the need for clinicians to communicate the cessation imperative. By using it, clinicians can help all smokers and non-smokers understand that there is no way to smoke tobacco without exposing friends and family.

 

Corresponding author: Jeremy E. Drehmer, MPH, 125 Nashua St., Suite 860, Boston, MA 02114, jdrehmer@ mgh.harvard.edu.

Financial disclosures: None

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19. Singer BC, Hodgson AT, Guevarra KS, et al. Gas-phase organics in environmental tobacco smoke. 1. Effects of smoking rate, ventilation, and furnishing level on emission factors. Env Sci Technol 2002;36:846–53.

20. Singer BC, Hodgson AT, Nazaroff WW. Gas-phase organics in environmental tobacco smoke: 2. Exposure-relevant emission factors and indirect exposures from habitual smoking. Atmos Environ 2003;37:5551–61.

21. Becquemin MH, Bertholon JF, Bentayeb M, et al. Third-hand smoking: indoor measurements of concentration and sizes of cigarette smoke particles after resuspension. Tob Control 2010;19:347–8.

22. Centers for Disease Control and Prevention [Internet]. How can we protect our children from secondhand smoke: a parent’s guide. Accessed 2017 Aug 15 at www.cdc.gov/tobacco/basic_information/secondhand_smoke/protect_children/pdfs/protect_children_guide.pdf.

23. Matt GE, Quintana PJ, Hovell MF, et al. Households contaminated by environmental tobacco smoke: sources of infant exposures. Tob Control 2004;13:29–37.

24. Matt GE, Quintana PJE, Zakarian JM, et al. When smokers move out and non-smokers move in: residential thirdhand smoke pollution and exposure. Tob Control 2011;20:e1.

25. Kraev TA, Adamkiewicz G, Hammond SK, Spengler JD. Indoor concentrations of nicotine in low-income, multi-unit housing: associations with smoking behaviours and housing characteristics. Tob Control 2009;18:438–44.

26. Matt GE, Quintana PJE, Hovell MF, et al. Residual tobacco smoke pollution in used cars for sale: air, dust, and surfaces. Nicotine Tob Res 2008;10:1467–75.

27. Matt GE, Quintana PJE, Fortmann AL, et al. Thirdhand smoke and exposure in California hotels: non-smoking rooms fail to protect non-smoking hotel guests from tobacco smoke exposure. Tob Control 2014;23:264–72.

28. Hang B, Sarker AH, Havel C, et al. Thirdhand smoke causes DNA damage in human cells. Mutagenesis 2013;28:381–91.

29. Mahabee-Gittens EM, Merianos AL, Matt GE. Preliminary evidence that high levels of nicotine on children’s hands may contribute to overall tobacco smoke exposure. Tob Control 2017 Mar 30.

30. Hovell MF, Zakarian JM, Matt GE, et al. Counseling to reduce children’s secondhand smoke exposure and help parents quit smoking: a controlled trial. Nicotine Tob Res 2009;11:1383–94.

31. Northrup TF, Khan AM, Jacob 3rd P, et al. Thirdhand smoke contamination in hospital settings: assessing exposure risk for vulnerable paediatric patients. Tob Control 2016; 25: 619–23.

32. Martins-Green M, Adhami N, Frankos M, et al. Cigarette smoke toxins deposited on surfaces: Implications for human health. PLoS One 2014;9:1–12.

33. Hang B, Snijders AM, Huang Y, et al. Early exposure to thirdhand cigarette smoke affects body mass and the development of immunity in mice. Sci Rep 2017;7:41915.

34. Northrup TF, Matt GE, Hovell MF, et al. Thirdhand smoke in the homes of medically fragile children: Assessing the impact of indoor smoking levels and smoking bans. Nicotine Tob Res 2016;18:1290–8.

35. Marbin JN, Purdy CN, Klaas K, et al. The Clinical Effort against Secondhand Smoke Exposure (CEASE) California: implementing a pediatric clinical intervention to reduce secondhand smoke exposure. Clin Pediatr (Phila) 2016;1(3).

36. Winickoff JP, Hipple B, Drehmer J, et al. The Clinical Effort Against Secondhand Smoke Exposure (CEASE) intervention: A decade of lessons learned. J Clin Outcomes Manag 2012;19:414–9.

37. Farber HJ, Groner J, Walley S, Nelson K. Protecting children from tobacco, nicotine, and tobacco smoke. Pediatrics 2015;136:e1439–67.

38. American Academy of Family Physicians [Internet]. AAFP policies. Tobacco use, prevention, and cessation. Accessed 2017 Aug 29 at www.aafp.org/about/policies/all/tobacco-smoking.html.

39. Farber HJ, Walley SC, Groner JA, et al. Clinical practice policy to protect children from tobacco, nicotine, and tobacco smoke. Pediatrics 2015;136:1008–17.

40. Drehmer J, Hipple B, Murphy S, Winickoff JP. EQIPP: Eliminating tobacco use and exposure to secondhand smoke [online course] PediaLink [Internet]. American Academy of Pediatrics. 2014. Available at bit.ly/eliminate-tobacco-responsive.

41. The American Academy of Pediatrics Julius B. Richmond Center of Excellence [Internet]. Accessed 2017 Aug 9 at www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/Richmond-Center/Pages/default.aspx.

42. Clinical Effort Against Secondhand Smoke Exposure [Internet]. Accessed at www.massgeneral.org/ceasetobacco/.

43. Winickoff JP, Nabi-Burza E, Chang Y, et al. Implementation of a parental tobacco control intervention in pediatric practice. Pediatrics 2013;132:109–17.

44. Drehmer JE, Ossip DJ, Nabi-Burza E, et al. Thirdhand smoke beliefs of parents. Pediatrics 2014;133:e850–6.

45. Drehmer JE, Ossip DJ, Rigotti NA, et al. Pediatrician interventions and thirdhand smoke beliefs of parents. Am J Prev Med 2012;43:533–6.

46. Samet JM, Chanson D, Wipfli H. The challenges of limiting exposure to THS in vulnerable populations. Curr Environ Health Rep 2015;2:215–25.

47. Thirdhand Smoke Research Consortium [Internet]. Accessed 2017 Aug 15 at www.trdrp.org/highlights-news-events/thirdhand-smoke-consortium.html.

48. Office of the Federal Register (US) [Internet]. Rule instituting smoke-free public housing. 2016. Available at www.federalregister.gov/documents/2016/12/05/2016-28986/instituting-smoke-free-public-housing.

References

1. Wynder EL, Graham EA, Croninger AB, et al. Experimental production of carcinoma with cigarette tar experimental production of carcinoma with cigarette tar. 1953;36:855–64.

2. Winickoff JP, Friebely J, Tanski SE, et al. Beliefs about the health effects of “thirdhand” smoke and home smoking bans. Pediatrics 2009;123:e74–9.

3. US Department of Health and Human Services. The health consequences of smoking- 50 years of progress: a report of the Surgeon General, Executive Summary. 2014.

4. World Health Organization. Tobacco fact sheet [Internet]. [cited 2017 Aug 15]. Available at www.who.int/mediacentre/factsheets/fs339/en/.

5. U.S. Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta (GA); 2006.

6. Winickoff J, Friebely J, Tanski S, et al. Beliefs about the health effects of third-hand smoke predict home and car smoking bans. In: Poster presented at the 2006 Pediatric Academic Societies Meeting. San Francisco, CA; 2006.

7. Tobacco-Related Disease Research Program [Internet]. Accessed 2017 Jul 7 at www.trdrp.org.

8. Matt GE, Quintana PJ, Destaillats H, et al. Thirdhand tobacco smoke: emerging evidence and arguments for a multidisciplinary research agenda. Environ Health Perspect 2011;119:1218–26.

9. Jacob P, Benowitz NL, Destaillats H, et al. Thirdhand smoke: new evidence, challenges, and future directions. Chem Res Toxicol 2017;30:270–94.

10. Roberts S, Hamill P. Grand Central: how a train station transformed America. Grand Central Publishing; 2013.

11. Sachs S. From gritty depot, a glittery destination; refurbished Grand Central terminal, worthy of its name, is reopened. New York Times 1998 Oct 2.

12. Grand Central: an engine of scientific innovation [Internet]. National Public Radio - Talk of the Nation; 2013. Available at www.npr.org/templates/transcript/transcript.php?storyId=175054273.

13. Lueck TJ. Work starts 100 feet above Grand Central commuters. New York Times 1996 Sep 20.

14. Van Loy MD, Nazaroff WW, Daisey JM. Nicotine as a marker for environmental tobacco smoke: implications of sorption on indoor surface materials. J Air Waste Manag Assoc 1998;48:959–68.

15. Sleiman M, Gundel LA, Pankow JF, et al. Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proc Natl Acad Sci U S A 2010;107:6576–81.

16. Xue J, Yang S, Seng S. Mechanisms of cancer induction by tobacco-specific NNK and NNN. Cancers (Basel) 2014;6:1138–56.

17. Ramirez N, Ozel MZ, Lewis AC, et al. Exposure to nitrosamines in thirdhand tobacco smoke increases cancer risk in non-smokers. Environ Int 2014;71:139–47.

18. Destaillats H, Singer BC, Lee SK, Gundel LA. Effect of ozone on nicotine desorption from model surfaces: evidence for heterogeneous chemistry. Environ Sci Technol 2006;40:1799–805.

19. Singer BC, Hodgson AT, Guevarra KS, et al. Gas-phase organics in environmental tobacco smoke. 1. Effects of smoking rate, ventilation, and furnishing level on emission factors. Env Sci Technol 2002;36:846–53.

20. Singer BC, Hodgson AT, Nazaroff WW. Gas-phase organics in environmental tobacco smoke: 2. Exposure-relevant emission factors and indirect exposures from habitual smoking. Atmos Environ 2003;37:5551–61.

21. Becquemin MH, Bertholon JF, Bentayeb M, et al. Third-hand smoking: indoor measurements of concentration and sizes of cigarette smoke particles after resuspension. Tob Control 2010;19:347–8.

22. Centers for Disease Control and Prevention [Internet]. How can we protect our children from secondhand smoke: a parent’s guide. Accessed 2017 Aug 15 at www.cdc.gov/tobacco/basic_information/secondhand_smoke/protect_children/pdfs/protect_children_guide.pdf.

23. Matt GE, Quintana PJ, Hovell MF, et al. Households contaminated by environmental tobacco smoke: sources of infant exposures. Tob Control 2004;13:29–37.

24. Matt GE, Quintana PJE, Zakarian JM, et al. When smokers move out and non-smokers move in: residential thirdhand smoke pollution and exposure. Tob Control 2011;20:e1.

25. Kraev TA, Adamkiewicz G, Hammond SK, Spengler JD. Indoor concentrations of nicotine in low-income, multi-unit housing: associations with smoking behaviours and housing characteristics. Tob Control 2009;18:438–44.

26. Matt GE, Quintana PJE, Hovell MF, et al. Residual tobacco smoke pollution in used cars for sale: air, dust, and surfaces. Nicotine Tob Res 2008;10:1467–75.

27. Matt GE, Quintana PJE, Fortmann AL, et al. Thirdhand smoke and exposure in California hotels: non-smoking rooms fail to protect non-smoking hotel guests from tobacco smoke exposure. Tob Control 2014;23:264–72.

28. Hang B, Sarker AH, Havel C, et al. Thirdhand smoke causes DNA damage in human cells. Mutagenesis 2013;28:381–91.

29. Mahabee-Gittens EM, Merianos AL, Matt GE. Preliminary evidence that high levels of nicotine on children’s hands may contribute to overall tobacco smoke exposure. Tob Control 2017 Mar 30.

30. Hovell MF, Zakarian JM, Matt GE, et al. Counseling to reduce children’s secondhand smoke exposure and help parents quit smoking: a controlled trial. Nicotine Tob Res 2009;11:1383–94.

31. Northrup TF, Khan AM, Jacob 3rd P, et al. Thirdhand smoke contamination in hospital settings: assessing exposure risk for vulnerable paediatric patients. Tob Control 2016; 25: 619–23.

32. Martins-Green M, Adhami N, Frankos M, et al. Cigarette smoke toxins deposited on surfaces: Implications for human health. PLoS One 2014;9:1–12.

33. Hang B, Snijders AM, Huang Y, et al. Early exposure to thirdhand cigarette smoke affects body mass and the development of immunity in mice. Sci Rep 2017;7:41915.

34. Northrup TF, Matt GE, Hovell MF, et al. Thirdhand smoke in the homes of medically fragile children: Assessing the impact of indoor smoking levels and smoking bans. Nicotine Tob Res 2016;18:1290–8.

35. Marbin JN, Purdy CN, Klaas K, et al. The Clinical Effort against Secondhand Smoke Exposure (CEASE) California: implementing a pediatric clinical intervention to reduce secondhand smoke exposure. Clin Pediatr (Phila) 2016;1(3).

36. Winickoff JP, Hipple B, Drehmer J, et al. The Clinical Effort Against Secondhand Smoke Exposure (CEASE) intervention: A decade of lessons learned. J Clin Outcomes Manag 2012;19:414–9.

37. Farber HJ, Groner J, Walley S, Nelson K. Protecting children from tobacco, nicotine, and tobacco smoke. Pediatrics 2015;136:e1439–67.

38. American Academy of Family Physicians [Internet]. AAFP policies. Tobacco use, prevention, and cessation. Accessed 2017 Aug 29 at www.aafp.org/about/policies/all/tobacco-smoking.html.

39. Farber HJ, Walley SC, Groner JA, et al. Clinical practice policy to protect children from tobacco, nicotine, and tobacco smoke. Pediatrics 2015;136:1008–17.

40. Drehmer J, Hipple B, Murphy S, Winickoff JP. EQIPP: Eliminating tobacco use and exposure to secondhand smoke [online course] PediaLink [Internet]. American Academy of Pediatrics. 2014. Available at bit.ly/eliminate-tobacco-responsive.

41. The American Academy of Pediatrics Julius B. Richmond Center of Excellence [Internet]. Accessed 2017 Aug 9 at www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/Richmond-Center/Pages/default.aspx.

42. Clinical Effort Against Secondhand Smoke Exposure [Internet]. Accessed at www.massgeneral.org/ceasetobacco/.

43. Winickoff JP, Nabi-Burza E, Chang Y, et al. Implementation of a parental tobacco control intervention in pediatric practice. Pediatrics 2013;132:109–17.

44. Drehmer JE, Ossip DJ, Nabi-Burza E, et al. Thirdhand smoke beliefs of parents. Pediatrics 2014;133:e850–6.

45. Drehmer JE, Ossip DJ, Rigotti NA, et al. Pediatrician interventions and thirdhand smoke beliefs of parents. Am J Prev Med 2012;43:533–6.

46. Samet JM, Chanson D, Wipfli H. The challenges of limiting exposure to THS in vulnerable populations. Curr Environ Health Rep 2015;2:215–25.

47. Thirdhand Smoke Research Consortium [Internet]. Accessed 2017 Aug 15 at www.trdrp.org/highlights-news-events/thirdhand-smoke-consortium.html.

48. Office of the Federal Register (US) [Internet]. Rule instituting smoke-free public housing. 2016. Available at www.federalregister.gov/documents/2016/12/05/2016-28986/instituting-smoke-free-public-housing.

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CDC Updates Guidance on Infants With Possible Zika Infection

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Testing and management may vary according to the infant’s clinical findings and the mother’s exposure to the virus.

Infants with possible prenatal exposure to Zika who test positive for the virus should receive an in-depth ophthalmologic exam, intensified hearing testing, and a thorough neurologic evaluation with brain imaging within one month of birth, according to new interim guidance from the Centers for Disease Control and Prevention (CDC).

The new clinical management guidelines, published in the October 20 issue of Morbidity and Mortality Weekly Report, supersede the CDC guidance issued in August 2016. The update was the product of a forum on the diagnosis, evaluation, and management of Zika in infants that the centers convened with the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists. Practicing clinicians and federal agency representatives reviewed the evolving body of knowledge on how best to care for these infants. Since Zika emerged as a public health concern, clinicians have reported postnatal onset of some symptoms, including eye abnormalities, incident microcephaly in infants with a normal head circumference at birth, EEG abnormalities, and diaphragmatic paralysis.

Tolulope Adebanjo, MD
“This updated interim guidance is based on current, limited data about Zika virus infection, the interpretation of individual expert opinion collected during the forum, and knowledge about other congenital infections, and reflects the information available as of September 2017,” according to Tolulope Adebanjo, MD, of the National Center for Immunization and Respiratory Diseases, at the CDC in Atlanta, and coauthors. “As more information becomes available, this guidance will be updated.”

Infants With Clinical Findings Consistent With Zika Syndrome

Infants with clinical findings consistent with congenital Zika syndrome who are born to mothers with possible Zika virus exposure in pregnancy should be tested for Zika virus with serum and urine tests. If those tests are negative, and there is no other apparent cause of the symptoms, they should have a CSF sample tested for Zika RNA and IgM Zika antibodies.

By one month, these infants should undergo a head ultrasound and a detailed ophthalmologic exam. The eye exam should pick up any anomalies of the anterior and posterior eye, including microphthalmia, coloboma, intraocular calcifications, optic nerve hypoplasia and atrophy, and macular scarring with focal pigmentary retinal mottling.

By one month, these infants also should undergo auditory brainstem response (ABR) audiometry, especially if the initial newborn hearing screen was done by otoacoustic emissions alone. Zika syndrome can include sensorineural hearing loss, although late-onset hearing loss has not been seen. Therefore, the follow-up ABR previously recommended at four to six months is no longer deemed necessary.

A comprehensive neurologic exam also is recommended. Seizures are sometimes part of Zika syndrome, but infants can also have subclinical EEG abnormalities. Advanced neuroimaging can identify obvious and subtle brain abnormalities, such as cortical thinning, corpus callosum abnormalities, calcifications at the junction of white and gray matter, and ventricular enlargement.

As infants grow, clinicians should be alert for signs of increased intracranial pressure that could signal postnatal hydrocephalus. Diaphragmatic paralysis also has been seen; it manifests as respiratory distress. Dysphagia that interferes with feeding can develop as well.

“The follow-up care of [these infants] requires a multidisciplinary team and an established medical home to facilitate the coordination of care and ensure that abnormal findings are addressed,” said Dr. Adebanjo and colleagues.

Asymptomatic Infants of Mothers With Possible Infection

Infants without clinical findings born to mothers with laboratory evidence of possible Zika virus infection during pregnancy should have the same early head ultrasound, hearing, and eye exams as those with clinical findings. All of these infants also should be tested for Zika virus just as those with clinical findings should be.

If tests are positive, these infants should have all the investigations and follow-up recommended for babies with clinical findings. If laboratory testing is negative, and clinical findings are normal, Zika infection is highly unlikely, and the infants can receive routine care. Clinicians and parents should be on the lookout, however, for new symptoms that might suggest postnatal Zika syndrome.

Asymptomatic Infants Whose Mothers Had Unconfirmed Zika Exposure

Infants without clinical findings consistent with congenital Zika syndrome born to mothers with possible Zika virus exposure in pregnancy, but without laboratory evidence of possible Zika virus infection during pregnancy, constitute a large group. Some women, for example, are never tested during pregnancy, and others have false negative test results. “Because the latter issues are not easily discerned, all mothers with possible exposure to Zika virus during pregnancy who do not have laboratory evidence of possible Zika virus infection, including those who tested negative with currently available technology, should be considered in this group,” said Dr. Adebanjo and colleagues.

 

 

The CDC do not recommend further Zika evaluation for these infants unless additional testing confirms maternal infection. For older infants, parents and clinicians should decide together whether further evaluations would be helpful. “If findings consistent with congenital Zika syndrome are identified at any time, referrals to the appropriate specialists should be made, and subsequent evaluation should follow recommendations for infants with clinical findings consistent with congenital Zika syndrome,” said the authors.

The CDC also reiterated their special recommendations for infants who had a prenatal diagnosis of Zika infection. For now, these recommendations remain unchanged, although “as more data become available, understanding of the diagnostic role of prenatal ultrasound and amniocentesis … will improve, and guidance will be updated.”

The optimal timing for a Zika diagnostic ultrasound is uncertain. The CDC recommend that serial ultrasounds be performed every three to four weeks for women with laboratory-confirmed prenatal Zika exposure. Women with possible exposure need only routine ultrasound screenings.

While Zika RNA has been identified in amniotic fluid, there is no consensus on the value of amniocentesis as a prenatal diagnostic tool. Investigations of serial amniocentesis suggest that viral shedding into the amniotic fluid might be transient. If amniocentesis is performed for other reasons, Zika nucleic acid testing can be incorporated.

A shared decision-making process about screening is key, said Dr. Adebanjo and colleagues. “For example, serial ultrasound examinations might be inconvenient, unpleasant, and expensive, and might prompt unnecessary interventions; amniocentesis carries additional known risks such as fetal loss. These potential harms of prenatal screening for congenital Zika syndrome might outweigh the clinical benefits for some patients; therefore, these decisions should be individualized.”

—Michele G. Sullivan

Suggested Reading

Adebanjo T, Godfred-Cato S, Viens L, et al. Update: Interim guidance for the diagnosis, evaluation, and management of infants with possible congenital Zika virus infection - United States, October 2017. MMWR Morb Mortal Wkly Rep. 2017;66(41):1089-1099.

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Testing and management may vary according to the infant’s clinical findings and the mother’s exposure to the virus.
Testing and management may vary according to the infant’s clinical findings and the mother’s exposure to the virus.

Infants with possible prenatal exposure to Zika who test positive for the virus should receive an in-depth ophthalmologic exam, intensified hearing testing, and a thorough neurologic evaluation with brain imaging within one month of birth, according to new interim guidance from the Centers for Disease Control and Prevention (CDC).

The new clinical management guidelines, published in the October 20 issue of Morbidity and Mortality Weekly Report, supersede the CDC guidance issued in August 2016. The update was the product of a forum on the diagnosis, evaluation, and management of Zika in infants that the centers convened with the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists. Practicing clinicians and federal agency representatives reviewed the evolving body of knowledge on how best to care for these infants. Since Zika emerged as a public health concern, clinicians have reported postnatal onset of some symptoms, including eye abnormalities, incident microcephaly in infants with a normal head circumference at birth, EEG abnormalities, and diaphragmatic paralysis.

Tolulope Adebanjo, MD
“This updated interim guidance is based on current, limited data about Zika virus infection, the interpretation of individual expert opinion collected during the forum, and knowledge about other congenital infections, and reflects the information available as of September 2017,” according to Tolulope Adebanjo, MD, of the National Center for Immunization and Respiratory Diseases, at the CDC in Atlanta, and coauthors. “As more information becomes available, this guidance will be updated.”

Infants With Clinical Findings Consistent With Zika Syndrome

Infants with clinical findings consistent with congenital Zika syndrome who are born to mothers with possible Zika virus exposure in pregnancy should be tested for Zika virus with serum and urine tests. If those tests are negative, and there is no other apparent cause of the symptoms, they should have a CSF sample tested for Zika RNA and IgM Zika antibodies.

By one month, these infants should undergo a head ultrasound and a detailed ophthalmologic exam. The eye exam should pick up any anomalies of the anterior and posterior eye, including microphthalmia, coloboma, intraocular calcifications, optic nerve hypoplasia and atrophy, and macular scarring with focal pigmentary retinal mottling.

By one month, these infants also should undergo auditory brainstem response (ABR) audiometry, especially if the initial newborn hearing screen was done by otoacoustic emissions alone. Zika syndrome can include sensorineural hearing loss, although late-onset hearing loss has not been seen. Therefore, the follow-up ABR previously recommended at four to six months is no longer deemed necessary.

A comprehensive neurologic exam also is recommended. Seizures are sometimes part of Zika syndrome, but infants can also have subclinical EEG abnormalities. Advanced neuroimaging can identify obvious and subtle brain abnormalities, such as cortical thinning, corpus callosum abnormalities, calcifications at the junction of white and gray matter, and ventricular enlargement.

As infants grow, clinicians should be alert for signs of increased intracranial pressure that could signal postnatal hydrocephalus. Diaphragmatic paralysis also has been seen; it manifests as respiratory distress. Dysphagia that interferes with feeding can develop as well.

“The follow-up care of [these infants] requires a multidisciplinary team and an established medical home to facilitate the coordination of care and ensure that abnormal findings are addressed,” said Dr. Adebanjo and colleagues.

Asymptomatic Infants of Mothers With Possible Infection

Infants without clinical findings born to mothers with laboratory evidence of possible Zika virus infection during pregnancy should have the same early head ultrasound, hearing, and eye exams as those with clinical findings. All of these infants also should be tested for Zika virus just as those with clinical findings should be.

If tests are positive, these infants should have all the investigations and follow-up recommended for babies with clinical findings. If laboratory testing is negative, and clinical findings are normal, Zika infection is highly unlikely, and the infants can receive routine care. Clinicians and parents should be on the lookout, however, for new symptoms that might suggest postnatal Zika syndrome.

Asymptomatic Infants Whose Mothers Had Unconfirmed Zika Exposure

Infants without clinical findings consistent with congenital Zika syndrome born to mothers with possible Zika virus exposure in pregnancy, but without laboratory evidence of possible Zika virus infection during pregnancy, constitute a large group. Some women, for example, are never tested during pregnancy, and others have false negative test results. “Because the latter issues are not easily discerned, all mothers with possible exposure to Zika virus during pregnancy who do not have laboratory evidence of possible Zika virus infection, including those who tested negative with currently available technology, should be considered in this group,” said Dr. Adebanjo and colleagues.

 

 

The CDC do not recommend further Zika evaluation for these infants unless additional testing confirms maternal infection. For older infants, parents and clinicians should decide together whether further evaluations would be helpful. “If findings consistent with congenital Zika syndrome are identified at any time, referrals to the appropriate specialists should be made, and subsequent evaluation should follow recommendations for infants with clinical findings consistent with congenital Zika syndrome,” said the authors.

The CDC also reiterated their special recommendations for infants who had a prenatal diagnosis of Zika infection. For now, these recommendations remain unchanged, although “as more data become available, understanding of the diagnostic role of prenatal ultrasound and amniocentesis … will improve, and guidance will be updated.”

The optimal timing for a Zika diagnostic ultrasound is uncertain. The CDC recommend that serial ultrasounds be performed every three to four weeks for women with laboratory-confirmed prenatal Zika exposure. Women with possible exposure need only routine ultrasound screenings.

While Zika RNA has been identified in amniotic fluid, there is no consensus on the value of amniocentesis as a prenatal diagnostic tool. Investigations of serial amniocentesis suggest that viral shedding into the amniotic fluid might be transient. If amniocentesis is performed for other reasons, Zika nucleic acid testing can be incorporated.

A shared decision-making process about screening is key, said Dr. Adebanjo and colleagues. “For example, serial ultrasound examinations might be inconvenient, unpleasant, and expensive, and might prompt unnecessary interventions; amniocentesis carries additional known risks such as fetal loss. These potential harms of prenatal screening for congenital Zika syndrome might outweigh the clinical benefits for some patients; therefore, these decisions should be individualized.”

—Michele G. Sullivan

Suggested Reading

Adebanjo T, Godfred-Cato S, Viens L, et al. Update: Interim guidance for the diagnosis, evaluation, and management of infants with possible congenital Zika virus infection - United States, October 2017. MMWR Morb Mortal Wkly Rep. 2017;66(41):1089-1099.

Infants with possible prenatal exposure to Zika who test positive for the virus should receive an in-depth ophthalmologic exam, intensified hearing testing, and a thorough neurologic evaluation with brain imaging within one month of birth, according to new interim guidance from the Centers for Disease Control and Prevention (CDC).

The new clinical management guidelines, published in the October 20 issue of Morbidity and Mortality Weekly Report, supersede the CDC guidance issued in August 2016. The update was the product of a forum on the diagnosis, evaluation, and management of Zika in infants that the centers convened with the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists. Practicing clinicians and federal agency representatives reviewed the evolving body of knowledge on how best to care for these infants. Since Zika emerged as a public health concern, clinicians have reported postnatal onset of some symptoms, including eye abnormalities, incident microcephaly in infants with a normal head circumference at birth, EEG abnormalities, and diaphragmatic paralysis.

Tolulope Adebanjo, MD
“This updated interim guidance is based on current, limited data about Zika virus infection, the interpretation of individual expert opinion collected during the forum, and knowledge about other congenital infections, and reflects the information available as of September 2017,” according to Tolulope Adebanjo, MD, of the National Center for Immunization and Respiratory Diseases, at the CDC in Atlanta, and coauthors. “As more information becomes available, this guidance will be updated.”

Infants With Clinical Findings Consistent With Zika Syndrome

Infants with clinical findings consistent with congenital Zika syndrome who are born to mothers with possible Zika virus exposure in pregnancy should be tested for Zika virus with serum and urine tests. If those tests are negative, and there is no other apparent cause of the symptoms, they should have a CSF sample tested for Zika RNA and IgM Zika antibodies.

By one month, these infants should undergo a head ultrasound and a detailed ophthalmologic exam. The eye exam should pick up any anomalies of the anterior and posterior eye, including microphthalmia, coloboma, intraocular calcifications, optic nerve hypoplasia and atrophy, and macular scarring with focal pigmentary retinal mottling.

By one month, these infants also should undergo auditory brainstem response (ABR) audiometry, especially if the initial newborn hearing screen was done by otoacoustic emissions alone. Zika syndrome can include sensorineural hearing loss, although late-onset hearing loss has not been seen. Therefore, the follow-up ABR previously recommended at four to six months is no longer deemed necessary.

A comprehensive neurologic exam also is recommended. Seizures are sometimes part of Zika syndrome, but infants can also have subclinical EEG abnormalities. Advanced neuroimaging can identify obvious and subtle brain abnormalities, such as cortical thinning, corpus callosum abnormalities, calcifications at the junction of white and gray matter, and ventricular enlargement.

As infants grow, clinicians should be alert for signs of increased intracranial pressure that could signal postnatal hydrocephalus. Diaphragmatic paralysis also has been seen; it manifests as respiratory distress. Dysphagia that interferes with feeding can develop as well.

“The follow-up care of [these infants] requires a multidisciplinary team and an established medical home to facilitate the coordination of care and ensure that abnormal findings are addressed,” said Dr. Adebanjo and colleagues.

Asymptomatic Infants of Mothers With Possible Infection

Infants without clinical findings born to mothers with laboratory evidence of possible Zika virus infection during pregnancy should have the same early head ultrasound, hearing, and eye exams as those with clinical findings. All of these infants also should be tested for Zika virus just as those with clinical findings should be.

If tests are positive, these infants should have all the investigations and follow-up recommended for babies with clinical findings. If laboratory testing is negative, and clinical findings are normal, Zika infection is highly unlikely, and the infants can receive routine care. Clinicians and parents should be on the lookout, however, for new symptoms that might suggest postnatal Zika syndrome.

Asymptomatic Infants Whose Mothers Had Unconfirmed Zika Exposure

Infants without clinical findings consistent with congenital Zika syndrome born to mothers with possible Zika virus exposure in pregnancy, but without laboratory evidence of possible Zika virus infection during pregnancy, constitute a large group. Some women, for example, are never tested during pregnancy, and others have false negative test results. “Because the latter issues are not easily discerned, all mothers with possible exposure to Zika virus during pregnancy who do not have laboratory evidence of possible Zika virus infection, including those who tested negative with currently available technology, should be considered in this group,” said Dr. Adebanjo and colleagues.

 

 

The CDC do not recommend further Zika evaluation for these infants unless additional testing confirms maternal infection. For older infants, parents and clinicians should decide together whether further evaluations would be helpful. “If findings consistent with congenital Zika syndrome are identified at any time, referrals to the appropriate specialists should be made, and subsequent evaluation should follow recommendations for infants with clinical findings consistent with congenital Zika syndrome,” said the authors.

The CDC also reiterated their special recommendations for infants who had a prenatal diagnosis of Zika infection. For now, these recommendations remain unchanged, although “as more data become available, understanding of the diagnostic role of prenatal ultrasound and amniocentesis … will improve, and guidance will be updated.”

The optimal timing for a Zika diagnostic ultrasound is uncertain. The CDC recommend that serial ultrasounds be performed every three to four weeks for women with laboratory-confirmed prenatal Zika exposure. Women with possible exposure need only routine ultrasound screenings.

While Zika RNA has been identified in amniotic fluid, there is no consensus on the value of amniocentesis as a prenatal diagnostic tool. Investigations of serial amniocentesis suggest that viral shedding into the amniotic fluid might be transient. If amniocentesis is performed for other reasons, Zika nucleic acid testing can be incorporated.

A shared decision-making process about screening is key, said Dr. Adebanjo and colleagues. “For example, serial ultrasound examinations might be inconvenient, unpleasant, and expensive, and might prompt unnecessary interventions; amniocentesis carries additional known risks such as fetal loss. These potential harms of prenatal screening for congenital Zika syndrome might outweigh the clinical benefits for some patients; therefore, these decisions should be individualized.”

—Michele G. Sullivan

Suggested Reading

Adebanjo T, Godfred-Cato S, Viens L, et al. Update: Interim guidance for the diagnosis, evaluation, and management of infants with possible congenital Zika virus infection - United States, October 2017. MMWR Morb Mortal Wkly Rep. 2017;66(41):1089-1099.

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What Are the Long-Term Neurologic Complications of Childhood Cancer?

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Most childhood cancer survivors have a chronic health problem by age 45.

KANSAS CITY, MO—As cancer treatment advances, the prevalence of childhood cancer survivors increases; as a result, physicians see more neurologic complications of surgery, chemotherapy, and radiation, according to an overview presented at the 46th Annual Meeting of the Child Neurology Society.  

Nicole Ullrich, MD, PhD

There is an increasing impact of neurologic and neuropsychological toxicity that underscores the need for intervention and follow-up over the lifespan, said Nicole Ullrich, MD, PhD, Director of Neurologic Neuro-Oncology at the Dana-Farber/Boston Children's Cancer and Blood Disorders Center.

Lifelong Effects

The prevalence of adult survivors of childhood cancer is one in 250 people, and there are more than 270,000 childhood cancer survivors in the United States. These cancer survivors experience long-term toxicities affecting their respiratory system, cardiovascular system, cerebrovascular system, reproductive system, and a gamut of other late effects of treatment that we need to think about as they continue to advance into adulthood, said Dr. Ullrich.

“Ninety-five percent of all cancer survivors will have a chronic health problem by the age of 45, and 80% will have a severe or life-threatening condition, she said. The risk is greater for patients with CNS malignancies.  

Childhood cancer survivors may develop physical, cognitive, and psychological issues later in life. These late effects have a significant impact on their quality and quantity of life. Neurologic issues can include headache, seizures, and stroke.

Headache and Seizures

Patients with elevated intracranial pressure or large tumors have an increased risk of headache. Nontumor causes of headache may include medications, such as antiemetic drugs and chemotherapy. Radiation therapy may cause acute radiation necrosis and long-term vascular issues. Supportive therapies, including steroids, antacids, and antinausea regimens, can cause headaches as well as sleep disruption, said Dr. Ullrich.

Approximately 15% to 25% of children with a brain tumor present with a seizure. Seizures are more often associated with low-grade tumors. Children with solid tumors or leukemia often have seizures without clinical or radiologic signs of a structural lesion. When a surgeon removes the tumor, there may be associated areas of dysplasia that surround the tumor, said Dr. Ullrich. Strategies such as electrocorticography or intraoperative monitoring can help identify epileptic zones for removal during surgery.

Potential causes of seizures include the tumor itself, surrounding edema, areas of cortical dysplasia, hyperexcitability related to neurotransmitters and glutamate levels, and scar formation that occurs after tumor resection. Individuals who have had cortically based or temporal lobe tumors or who have had incomplete resection or preexisting seizures before diagnosis have the highest risk of developing seizures, even years after completion of therapy.

EEG can help confirm seizures and distinguish between seizure types. It also can aid in the choice of an anticonvulsant. “We tend to lean more towards non-enzyme-inducing anticonvulsants in order to not interfere with concurrent chemotherapy,” said Dr. Ullrich. If seizures are acutely related to a drug or infection, Dr. Ullrich aims to withdraw anticonvulsants as soon as possible.

Surgery and Chemotherapy

Children who have had a gross total resection of the primary tumor may still be at risk for acute neurologic, neurosensory, and neuromotor issues, endocrine dysfunction, cerebellar mutism, and other neuropsychological deficits, said Dr. Ullrich.

Deficits and long-term effects of brain tumor treatment mainly depend on tumor location. Maximal tumor resection may cause hypopituitarism, vascular issues, and vision issues. Image-guided therapy can help surgeons remove most, if not all, of the tumor during the initial resection.  

Chemotherapy-related neurologic effects are common, said Dr. Ullrich. One of the main side effects is chemotherapy-induced peripheral neuropathy (ie, any injury or inflammation to the peripheral nerve due to administration of a chemotherapeutic drug). Patients with peripheral neuropathy may exhibit changes in their gait, loss of reflexes, and sensory changes. Pediatric patients with Charcot-Marie-Tooth disease or other hereditary neuropathies have a greater risk of chemotherapy-induced peripheral neuropathy.

Radiation

Age at the time of radiation, radiation field, genetic predisposition, and total dose are all risk factors for radiation-induced cognitive injury. One study found that children younger than 7 had the most significant decline in overall IQ after radiation. This research led to a shift in the development of treatment protocols and inspired physicians to strive to decrease and eliminate the use of radiation in the youngest patients, said Dr. Ullrich.

Another consequence of radiation may be the development of secondary neoplasms. The mean interval between the time of radiation and the development of secondary tumors is around eight years. These secondary neoplasms resulting from radiation often have anaplastic features. Childhood cancer survivors should see a dermatologist to monitor radiated areas for skin cancer.

 

 

Stroke and SMART Syndrome

Stroke is increasingly recognized as a late consequence of cancer treatment, especially in patients who have been treated for leukemia and brain tumors. Studies have found that prior radiation is an independent predictor of stroke. Mueller et al found that pediatric cancer survivors with hypertension had a fourfold increased risk of stroke, compared with sibling controls.

“Screen for correctable risk factors such as hypertension, hypercholesterolemia, hyperlipidemia, obesity, and sedentary lifestyle, said Dr. Ullrich.

SMART syndrome (stroke-like migraine attacks after radiation therapy) is another potential complication that can occur years after radiation therapy. The syndrome can present like a transient ischemic attack, and symptoms can last hours to days. This syndrome can be treated with aggressive preventive headache care.  

Mitigation and Prevention

Neurologists can take steps to help prevent or ameliorate some of these late effects. The Children's Oncology Group has created Passport for Care, a tool that allows patients to share a summary of their cancer treatments and follow-up recommendations with their primary care providers. The Children's Oncology Group also has created long-term follow-up guidelines for survivors of childhood, adolescent, and young adult cancers.

In addition, new and refined surgical techniques help detect and remove residual tumor after surgery. Proton beam radiation, intensity-modulated radiation therapy, and other approaches can help reduce doses of radiation, potentially reducing cognitive risks. The goal is to shift the paradigm from just categorizing the late effects to mitigating them and actually preventing them in the first place, said Dr. Ullrich.

—Erica Tricarico

Suggested Reading

Mueller S, Fullerton HJ, Stratton K, et al. Radiation, atherosclerotic risk factors and stroke risk in survivors of pediatric cancer: a report from the Childhood Cancer Survivor Study. Int J Radiat Oncol Biol Phys. 2013;86(4):649-655.

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Most childhood cancer survivors have a chronic health problem by age 45.
Most childhood cancer survivors have a chronic health problem by age 45.

KANSAS CITY, MO—As cancer treatment advances, the prevalence of childhood cancer survivors increases; as a result, physicians see more neurologic complications of surgery, chemotherapy, and radiation, according to an overview presented at the 46th Annual Meeting of the Child Neurology Society.  

Nicole Ullrich, MD, PhD

There is an increasing impact of neurologic and neuropsychological toxicity that underscores the need for intervention and follow-up over the lifespan, said Nicole Ullrich, MD, PhD, Director of Neurologic Neuro-Oncology at the Dana-Farber/Boston Children's Cancer and Blood Disorders Center.

Lifelong Effects

The prevalence of adult survivors of childhood cancer is one in 250 people, and there are more than 270,000 childhood cancer survivors in the United States. These cancer survivors experience long-term toxicities affecting their respiratory system, cardiovascular system, cerebrovascular system, reproductive system, and a gamut of other late effects of treatment that we need to think about as they continue to advance into adulthood, said Dr. Ullrich.

“Ninety-five percent of all cancer survivors will have a chronic health problem by the age of 45, and 80% will have a severe or life-threatening condition, she said. The risk is greater for patients with CNS malignancies.  

Childhood cancer survivors may develop physical, cognitive, and psychological issues later in life. These late effects have a significant impact on their quality and quantity of life. Neurologic issues can include headache, seizures, and stroke.

Headache and Seizures

Patients with elevated intracranial pressure or large tumors have an increased risk of headache. Nontumor causes of headache may include medications, such as antiemetic drugs and chemotherapy. Radiation therapy may cause acute radiation necrosis and long-term vascular issues. Supportive therapies, including steroids, antacids, and antinausea regimens, can cause headaches as well as sleep disruption, said Dr. Ullrich.

Approximately 15% to 25% of children with a brain tumor present with a seizure. Seizures are more often associated with low-grade tumors. Children with solid tumors or leukemia often have seizures without clinical or radiologic signs of a structural lesion. When a surgeon removes the tumor, there may be associated areas of dysplasia that surround the tumor, said Dr. Ullrich. Strategies such as electrocorticography or intraoperative monitoring can help identify epileptic zones for removal during surgery.

Potential causes of seizures include the tumor itself, surrounding edema, areas of cortical dysplasia, hyperexcitability related to neurotransmitters and glutamate levels, and scar formation that occurs after tumor resection. Individuals who have had cortically based or temporal lobe tumors or who have had incomplete resection or preexisting seizures before diagnosis have the highest risk of developing seizures, even years after completion of therapy.

EEG can help confirm seizures and distinguish between seizure types. It also can aid in the choice of an anticonvulsant. “We tend to lean more towards non-enzyme-inducing anticonvulsants in order to not interfere with concurrent chemotherapy,” said Dr. Ullrich. If seizures are acutely related to a drug or infection, Dr. Ullrich aims to withdraw anticonvulsants as soon as possible.

Surgery and Chemotherapy

Children who have had a gross total resection of the primary tumor may still be at risk for acute neurologic, neurosensory, and neuromotor issues, endocrine dysfunction, cerebellar mutism, and other neuropsychological deficits, said Dr. Ullrich.

Deficits and long-term effects of brain tumor treatment mainly depend on tumor location. Maximal tumor resection may cause hypopituitarism, vascular issues, and vision issues. Image-guided therapy can help surgeons remove most, if not all, of the tumor during the initial resection.  

Chemotherapy-related neurologic effects are common, said Dr. Ullrich. One of the main side effects is chemotherapy-induced peripheral neuropathy (ie, any injury or inflammation to the peripheral nerve due to administration of a chemotherapeutic drug). Patients with peripheral neuropathy may exhibit changes in their gait, loss of reflexes, and sensory changes. Pediatric patients with Charcot-Marie-Tooth disease or other hereditary neuropathies have a greater risk of chemotherapy-induced peripheral neuropathy.

Radiation

Age at the time of radiation, radiation field, genetic predisposition, and total dose are all risk factors for radiation-induced cognitive injury. One study found that children younger than 7 had the most significant decline in overall IQ after radiation. This research led to a shift in the development of treatment protocols and inspired physicians to strive to decrease and eliminate the use of radiation in the youngest patients, said Dr. Ullrich.

Another consequence of radiation may be the development of secondary neoplasms. The mean interval between the time of radiation and the development of secondary tumors is around eight years. These secondary neoplasms resulting from radiation often have anaplastic features. Childhood cancer survivors should see a dermatologist to monitor radiated areas for skin cancer.

 

 

Stroke and SMART Syndrome

Stroke is increasingly recognized as a late consequence of cancer treatment, especially in patients who have been treated for leukemia and brain tumors. Studies have found that prior radiation is an independent predictor of stroke. Mueller et al found that pediatric cancer survivors with hypertension had a fourfold increased risk of stroke, compared with sibling controls.

“Screen for correctable risk factors such as hypertension, hypercholesterolemia, hyperlipidemia, obesity, and sedentary lifestyle, said Dr. Ullrich.

SMART syndrome (stroke-like migraine attacks after radiation therapy) is another potential complication that can occur years after radiation therapy. The syndrome can present like a transient ischemic attack, and symptoms can last hours to days. This syndrome can be treated with aggressive preventive headache care.  

Mitigation and Prevention

Neurologists can take steps to help prevent or ameliorate some of these late effects. The Children's Oncology Group has created Passport for Care, a tool that allows patients to share a summary of their cancer treatments and follow-up recommendations with their primary care providers. The Children's Oncology Group also has created long-term follow-up guidelines for survivors of childhood, adolescent, and young adult cancers.

In addition, new and refined surgical techniques help detect and remove residual tumor after surgery. Proton beam radiation, intensity-modulated radiation therapy, and other approaches can help reduce doses of radiation, potentially reducing cognitive risks. The goal is to shift the paradigm from just categorizing the late effects to mitigating them and actually preventing them in the first place, said Dr. Ullrich.

—Erica Tricarico

Suggested Reading

Mueller S, Fullerton HJ, Stratton K, et al. Radiation, atherosclerotic risk factors and stroke risk in survivors of pediatric cancer: a report from the Childhood Cancer Survivor Study. Int J Radiat Oncol Biol Phys. 2013;86(4):649-655.

KANSAS CITY, MO—As cancer treatment advances, the prevalence of childhood cancer survivors increases; as a result, physicians see more neurologic complications of surgery, chemotherapy, and radiation, according to an overview presented at the 46th Annual Meeting of the Child Neurology Society.  

Nicole Ullrich, MD, PhD

There is an increasing impact of neurologic and neuropsychological toxicity that underscores the need for intervention and follow-up over the lifespan, said Nicole Ullrich, MD, PhD, Director of Neurologic Neuro-Oncology at the Dana-Farber/Boston Children's Cancer and Blood Disorders Center.

Lifelong Effects

The prevalence of adult survivors of childhood cancer is one in 250 people, and there are more than 270,000 childhood cancer survivors in the United States. These cancer survivors experience long-term toxicities affecting their respiratory system, cardiovascular system, cerebrovascular system, reproductive system, and a gamut of other late effects of treatment that we need to think about as they continue to advance into adulthood, said Dr. Ullrich.

“Ninety-five percent of all cancer survivors will have a chronic health problem by the age of 45, and 80% will have a severe or life-threatening condition, she said. The risk is greater for patients with CNS malignancies.  

Childhood cancer survivors may develop physical, cognitive, and psychological issues later in life. These late effects have a significant impact on their quality and quantity of life. Neurologic issues can include headache, seizures, and stroke.

Headache and Seizures

Patients with elevated intracranial pressure or large tumors have an increased risk of headache. Nontumor causes of headache may include medications, such as antiemetic drugs and chemotherapy. Radiation therapy may cause acute radiation necrosis and long-term vascular issues. Supportive therapies, including steroids, antacids, and antinausea regimens, can cause headaches as well as sleep disruption, said Dr. Ullrich.

Approximately 15% to 25% of children with a brain tumor present with a seizure. Seizures are more often associated with low-grade tumors. Children with solid tumors or leukemia often have seizures without clinical or radiologic signs of a structural lesion. When a surgeon removes the tumor, there may be associated areas of dysplasia that surround the tumor, said Dr. Ullrich. Strategies such as electrocorticography or intraoperative monitoring can help identify epileptic zones for removal during surgery.

Potential causes of seizures include the tumor itself, surrounding edema, areas of cortical dysplasia, hyperexcitability related to neurotransmitters and glutamate levels, and scar formation that occurs after tumor resection. Individuals who have had cortically based or temporal lobe tumors or who have had incomplete resection or preexisting seizures before diagnosis have the highest risk of developing seizures, even years after completion of therapy.

EEG can help confirm seizures and distinguish between seizure types. It also can aid in the choice of an anticonvulsant. “We tend to lean more towards non-enzyme-inducing anticonvulsants in order to not interfere with concurrent chemotherapy,” said Dr. Ullrich. If seizures are acutely related to a drug or infection, Dr. Ullrich aims to withdraw anticonvulsants as soon as possible.

Surgery and Chemotherapy

Children who have had a gross total resection of the primary tumor may still be at risk for acute neurologic, neurosensory, and neuromotor issues, endocrine dysfunction, cerebellar mutism, and other neuropsychological deficits, said Dr. Ullrich.

Deficits and long-term effects of brain tumor treatment mainly depend on tumor location. Maximal tumor resection may cause hypopituitarism, vascular issues, and vision issues. Image-guided therapy can help surgeons remove most, if not all, of the tumor during the initial resection.  

Chemotherapy-related neurologic effects are common, said Dr. Ullrich. One of the main side effects is chemotherapy-induced peripheral neuropathy (ie, any injury or inflammation to the peripheral nerve due to administration of a chemotherapeutic drug). Patients with peripheral neuropathy may exhibit changes in their gait, loss of reflexes, and sensory changes. Pediatric patients with Charcot-Marie-Tooth disease or other hereditary neuropathies have a greater risk of chemotherapy-induced peripheral neuropathy.

Radiation

Age at the time of radiation, radiation field, genetic predisposition, and total dose are all risk factors for radiation-induced cognitive injury. One study found that children younger than 7 had the most significant decline in overall IQ after radiation. This research led to a shift in the development of treatment protocols and inspired physicians to strive to decrease and eliminate the use of radiation in the youngest patients, said Dr. Ullrich.

Another consequence of radiation may be the development of secondary neoplasms. The mean interval between the time of radiation and the development of secondary tumors is around eight years. These secondary neoplasms resulting from radiation often have anaplastic features. Childhood cancer survivors should see a dermatologist to monitor radiated areas for skin cancer.

 

 

Stroke and SMART Syndrome

Stroke is increasingly recognized as a late consequence of cancer treatment, especially in patients who have been treated for leukemia and brain tumors. Studies have found that prior radiation is an independent predictor of stroke. Mueller et al found that pediatric cancer survivors with hypertension had a fourfold increased risk of stroke, compared with sibling controls.

“Screen for correctable risk factors such as hypertension, hypercholesterolemia, hyperlipidemia, obesity, and sedentary lifestyle, said Dr. Ullrich.

SMART syndrome (stroke-like migraine attacks after radiation therapy) is another potential complication that can occur years after radiation therapy. The syndrome can present like a transient ischemic attack, and symptoms can last hours to days. This syndrome can be treated with aggressive preventive headache care.  

Mitigation and Prevention

Neurologists can take steps to help prevent or ameliorate some of these late effects. The Children's Oncology Group has created Passport for Care, a tool that allows patients to share a summary of their cancer treatments and follow-up recommendations with their primary care providers. The Children's Oncology Group also has created long-term follow-up guidelines for survivors of childhood, adolescent, and young adult cancers.

In addition, new and refined surgical techniques help detect and remove residual tumor after surgery. Proton beam radiation, intensity-modulated radiation therapy, and other approaches can help reduce doses of radiation, potentially reducing cognitive risks. The goal is to shift the paradigm from just categorizing the late effects to mitigating them and actually preventing them in the first place, said Dr. Ullrich.

—Erica Tricarico

Suggested Reading

Mueller S, Fullerton HJ, Stratton K, et al. Radiation, atherosclerotic risk factors and stroke risk in survivors of pediatric cancer: a report from the Childhood Cancer Survivor Study. Int J Radiat Oncol Biol Phys. 2013;86(4):649-655.

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Confluent and reticulated papillomatosis

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Confluent and reticulated papillomatosis of Gougerot and Carteaud, also known as Gougerot-Carteaud syndrome, is an uncommon skin disorder of young individuals characterized by hyperkeratotic or verrucous brown papules or plaques that coalesce centrally and by a reticulated pattern peripherally. It was first described by two French dermatologists, Gougerot and Carteaud, in 1927.1 Initially, the distinct entity of CARP was contested, with some dermatologists believing it to be a variant of acanthosis nigricans. However, CARP is now recognized as a distinct, though rare, dermatosis.

Dr. Lawrence F. Eichenfield
CARP commonly affects teens and young adults, with a mean age of onset of 15 years and without gender predilection.2The most common skin findings of CARP are somewhat verrucous or slightly hyperkeratotic brown papules a few millimeters in diameter. They are closely set together to form plaques in the center of the involved area, while those on the periphery of the involved area form a characteristic reticulated pattern. Papules are often scaly, although verrucous papules, especially those found in intertriginous areas, may develop a velvety appearance. Macules and patches may be present as well. The most common areas of involvement include the central chest and back with lesions extending in a rhomboidal fashion superoinferiorly, as well as the neck and axillae.1 Uncommonly, pubic and facial skin may be affected.2 Skin lesions are frequently hyperpigmented; however, cases of hypopigmented variants have been reported in darker-skinned individuals, although these cases have often been misdiagnosed as tinea versicolor.3 The majority of patients are asymptomatic, although some report mild pruritus. Care often is sought for cosmetic concerns.

Histopathology reveals findings similar to those that may be found in acanthosis nigricans and epidermal nevi. Classic characteristics of CARP include hyperkeratosis, papillomatosis, increased basal melanin pigmentation, and mild acanthosis. Occasionally, there may be perivascular lymphocytic infiltrates in the superficial dermis.3,4

The etiology of CARP is unknown. CARP’s resolution in response to antibiotics and the isolation of two bacterial actinomycetes, Rhodococcus and Dietzia papillomatosis, from skin scrapings of CARP patients have led some to believe that its etiology is bacterial. However, no bacterial species have been consistently isolated from CARP patients. The prevailing theory of the past was that CARP was an abnormal host response to the fungus Malassezia furfur. Inconsistent detection of the fungus in skin scrapings, as well as persistence of the skin lesions after fungal clearance with antifungal therapy, has debunked this theory. An underlying disorder of keratinization resulting in hyperproliferation also has been suggested given reports of familial CARP and electron microscopy studies demonstrating focal-enhanced expression of keratin-16 in the stratum granulosom.5 Other theories include a cutaneous response to underlying endocrinopathies, ultraviolet light, and localized amyloidosis.1
 

Diagnosis and differential

CARP is poorly recognized by clinicians and frequently initially misdiagnosed due to its similar appearance to other disorders, most commonly tinea versicolor and acanthosis nigricans. Davis et al. proposed criteria for diagnosis of CARP requiring 1) presence of scaly, reticulated and papillomatous brown macules and patches; 2) distribution over the upper trunk and neck; 3) negative fungal staining of scales; 4) no improvement following antifungal treatment; and 5) improvement following minocycline.2

Tinea versicolor may appear similar to CARP, but unlike CARP, will respond to antifungal treatment and may demonstrate hyphae and yeast on KOH preparation. Acanthosis nigricans and CARP both may present with velvety, hyperpigmented plaques in individuals of obese habitus or with insulin resistance, but peripheral reticulation will be absent in acanthosis nigricans. However, acanthosis nigricans and CARP may coexist, and this coexistence is not uncommonly seen in individuals with obesity and/or insulin resistance. Darier’s disease may look similar to cases of CARP without pigmentary change, but it often will have accompanying nail changes. Macular or lichen amyloidosis may present with pruritic brown macules or papules, but skin biopsy will have positive amyloid staining. The use of 70% alcohol swabbing to diagnose terra firma-forme dermatosis, with lesions disappearing with swabbing, is classic and used to differentiate it from CARP. Other conditions to consider include seborrheic dermatitis, epidermal nevi, verruca plana, epidermodysplasia verruciformis, and acne vulgaris.1,2,4
 

Treatment

Minocycline is the first-line treatment for CARP: 80% of patients may have complete resolution with minocycline, while the remainder experience at least 50% clearance of skin lesions.2 However, recurrence after stopping minocycline treatment is not uncommon. The mechanism by which minocycline works is unknown. Second-line treatment for those who cannot tolerate minocycline are macrolide antibiotics.6 Other treatment options with reported success include oral isotretinoin and topical retinoids, including tretinoin gel and tazarotene cream.3,7 Appropriate strength topical corticosteroids may be used for pruritus.

Allison Han

Ms. Han is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, as well as the vice chair of the department of dermatology and a professor of dermatology and pediatrics at UC San Diego. They report having no conflicts of interest or financial disclosures. Email them at pdnews@frontlinemedcom.com.

Dr. Lawrence F. Eichenfield

References

1. Clin Cosmet Investig Dermatol. 2016 Aug 25;9:217-23.

2. Br J Dermatol. 2006 Feb;154(2):287-93.

3. Arch Dermatol. 2012 Apr;148(4):505-8.

4. J Am Acad Dermatol. 2003 Dec;49(6):1182-4.

5. Arch Dermatol. 2002 Feb;138(2):276-7.

6. J Am Acad Dermatol. 2001;44(4):652-5.

7. Am J Clin Dermatol. 2006;7(5):305-13.
 

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Confluent and reticulated papillomatosis of Gougerot and Carteaud, also known as Gougerot-Carteaud syndrome, is an uncommon skin disorder of young individuals characterized by hyperkeratotic or verrucous brown papules or plaques that coalesce centrally and by a reticulated pattern peripherally. It was first described by two French dermatologists, Gougerot and Carteaud, in 1927.1 Initially, the distinct entity of CARP was contested, with some dermatologists believing it to be a variant of acanthosis nigricans. However, CARP is now recognized as a distinct, though rare, dermatosis.

Dr. Lawrence F. Eichenfield
CARP commonly affects teens and young adults, with a mean age of onset of 15 years and without gender predilection.2The most common skin findings of CARP are somewhat verrucous or slightly hyperkeratotic brown papules a few millimeters in diameter. They are closely set together to form plaques in the center of the involved area, while those on the periphery of the involved area form a characteristic reticulated pattern. Papules are often scaly, although verrucous papules, especially those found in intertriginous areas, may develop a velvety appearance. Macules and patches may be present as well. The most common areas of involvement include the central chest and back with lesions extending in a rhomboidal fashion superoinferiorly, as well as the neck and axillae.1 Uncommonly, pubic and facial skin may be affected.2 Skin lesions are frequently hyperpigmented; however, cases of hypopigmented variants have been reported in darker-skinned individuals, although these cases have often been misdiagnosed as tinea versicolor.3 The majority of patients are asymptomatic, although some report mild pruritus. Care often is sought for cosmetic concerns.

Histopathology reveals findings similar to those that may be found in acanthosis nigricans and epidermal nevi. Classic characteristics of CARP include hyperkeratosis, papillomatosis, increased basal melanin pigmentation, and mild acanthosis. Occasionally, there may be perivascular lymphocytic infiltrates in the superficial dermis.3,4

The etiology of CARP is unknown. CARP’s resolution in response to antibiotics and the isolation of two bacterial actinomycetes, Rhodococcus and Dietzia papillomatosis, from skin scrapings of CARP patients have led some to believe that its etiology is bacterial. However, no bacterial species have been consistently isolated from CARP patients. The prevailing theory of the past was that CARP was an abnormal host response to the fungus Malassezia furfur. Inconsistent detection of the fungus in skin scrapings, as well as persistence of the skin lesions after fungal clearance with antifungal therapy, has debunked this theory. An underlying disorder of keratinization resulting in hyperproliferation also has been suggested given reports of familial CARP and electron microscopy studies demonstrating focal-enhanced expression of keratin-16 in the stratum granulosom.5 Other theories include a cutaneous response to underlying endocrinopathies, ultraviolet light, and localized amyloidosis.1
 

Diagnosis and differential

CARP is poorly recognized by clinicians and frequently initially misdiagnosed due to its similar appearance to other disorders, most commonly tinea versicolor and acanthosis nigricans. Davis et al. proposed criteria for diagnosis of CARP requiring 1) presence of scaly, reticulated and papillomatous brown macules and patches; 2) distribution over the upper trunk and neck; 3) negative fungal staining of scales; 4) no improvement following antifungal treatment; and 5) improvement following minocycline.2

Tinea versicolor may appear similar to CARP, but unlike CARP, will respond to antifungal treatment and may demonstrate hyphae and yeast on KOH preparation. Acanthosis nigricans and CARP both may present with velvety, hyperpigmented plaques in individuals of obese habitus or with insulin resistance, but peripheral reticulation will be absent in acanthosis nigricans. However, acanthosis nigricans and CARP may coexist, and this coexistence is not uncommonly seen in individuals with obesity and/or insulin resistance. Darier’s disease may look similar to cases of CARP without pigmentary change, but it often will have accompanying nail changes. Macular or lichen amyloidosis may present with pruritic brown macules or papules, but skin biopsy will have positive amyloid staining. The use of 70% alcohol swabbing to diagnose terra firma-forme dermatosis, with lesions disappearing with swabbing, is classic and used to differentiate it from CARP. Other conditions to consider include seborrheic dermatitis, epidermal nevi, verruca plana, epidermodysplasia verruciformis, and acne vulgaris.1,2,4
 

Treatment

Minocycline is the first-line treatment for CARP: 80% of patients may have complete resolution with minocycline, while the remainder experience at least 50% clearance of skin lesions.2 However, recurrence after stopping minocycline treatment is not uncommon. The mechanism by which minocycline works is unknown. Second-line treatment for those who cannot tolerate minocycline are macrolide antibiotics.6 Other treatment options with reported success include oral isotretinoin and topical retinoids, including tretinoin gel and tazarotene cream.3,7 Appropriate strength topical corticosteroids may be used for pruritus.

Allison Han

Ms. Han is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, as well as the vice chair of the department of dermatology and a professor of dermatology and pediatrics at UC San Diego. They report having no conflicts of interest or financial disclosures. Email them at pdnews@frontlinemedcom.com.

Dr. Lawrence F. Eichenfield

References

1. Clin Cosmet Investig Dermatol. 2016 Aug 25;9:217-23.

2. Br J Dermatol. 2006 Feb;154(2):287-93.

3. Arch Dermatol. 2012 Apr;148(4):505-8.

4. J Am Acad Dermatol. 2003 Dec;49(6):1182-4.

5. Arch Dermatol. 2002 Feb;138(2):276-7.

6. J Am Acad Dermatol. 2001;44(4):652-5.

7. Am J Clin Dermatol. 2006;7(5):305-13.
 

 

Confluent and reticulated papillomatosis of Gougerot and Carteaud, also known as Gougerot-Carteaud syndrome, is an uncommon skin disorder of young individuals characterized by hyperkeratotic or verrucous brown papules or plaques that coalesce centrally and by a reticulated pattern peripherally. It was first described by two French dermatologists, Gougerot and Carteaud, in 1927.1 Initially, the distinct entity of CARP was contested, with some dermatologists believing it to be a variant of acanthosis nigricans. However, CARP is now recognized as a distinct, though rare, dermatosis.

Dr. Lawrence F. Eichenfield
CARP commonly affects teens and young adults, with a mean age of onset of 15 years and without gender predilection.2The most common skin findings of CARP are somewhat verrucous or slightly hyperkeratotic brown papules a few millimeters in diameter. They are closely set together to form plaques in the center of the involved area, while those on the periphery of the involved area form a characteristic reticulated pattern. Papules are often scaly, although verrucous papules, especially those found in intertriginous areas, may develop a velvety appearance. Macules and patches may be present as well. The most common areas of involvement include the central chest and back with lesions extending in a rhomboidal fashion superoinferiorly, as well as the neck and axillae.1 Uncommonly, pubic and facial skin may be affected.2 Skin lesions are frequently hyperpigmented; however, cases of hypopigmented variants have been reported in darker-skinned individuals, although these cases have often been misdiagnosed as tinea versicolor.3 The majority of patients are asymptomatic, although some report mild pruritus. Care often is sought for cosmetic concerns.

Histopathology reveals findings similar to those that may be found in acanthosis nigricans and epidermal nevi. Classic characteristics of CARP include hyperkeratosis, papillomatosis, increased basal melanin pigmentation, and mild acanthosis. Occasionally, there may be perivascular lymphocytic infiltrates in the superficial dermis.3,4

The etiology of CARP is unknown. CARP’s resolution in response to antibiotics and the isolation of two bacterial actinomycetes, Rhodococcus and Dietzia papillomatosis, from skin scrapings of CARP patients have led some to believe that its etiology is bacterial. However, no bacterial species have been consistently isolated from CARP patients. The prevailing theory of the past was that CARP was an abnormal host response to the fungus Malassezia furfur. Inconsistent detection of the fungus in skin scrapings, as well as persistence of the skin lesions after fungal clearance with antifungal therapy, has debunked this theory. An underlying disorder of keratinization resulting in hyperproliferation also has been suggested given reports of familial CARP and electron microscopy studies demonstrating focal-enhanced expression of keratin-16 in the stratum granulosom.5 Other theories include a cutaneous response to underlying endocrinopathies, ultraviolet light, and localized amyloidosis.1
 

Diagnosis and differential

CARP is poorly recognized by clinicians and frequently initially misdiagnosed due to its similar appearance to other disorders, most commonly tinea versicolor and acanthosis nigricans. Davis et al. proposed criteria for diagnosis of CARP requiring 1) presence of scaly, reticulated and papillomatous brown macules and patches; 2) distribution over the upper trunk and neck; 3) negative fungal staining of scales; 4) no improvement following antifungal treatment; and 5) improvement following minocycline.2

Tinea versicolor may appear similar to CARP, but unlike CARP, will respond to antifungal treatment and may demonstrate hyphae and yeast on KOH preparation. Acanthosis nigricans and CARP both may present with velvety, hyperpigmented plaques in individuals of obese habitus or with insulin resistance, but peripheral reticulation will be absent in acanthosis nigricans. However, acanthosis nigricans and CARP may coexist, and this coexistence is not uncommonly seen in individuals with obesity and/or insulin resistance. Darier’s disease may look similar to cases of CARP without pigmentary change, but it often will have accompanying nail changes. Macular or lichen amyloidosis may present with pruritic brown macules or papules, but skin biopsy will have positive amyloid staining. The use of 70% alcohol swabbing to diagnose terra firma-forme dermatosis, with lesions disappearing with swabbing, is classic and used to differentiate it from CARP. Other conditions to consider include seborrheic dermatitis, epidermal nevi, verruca plana, epidermodysplasia verruciformis, and acne vulgaris.1,2,4
 

Treatment

Minocycline is the first-line treatment for CARP: 80% of patients may have complete resolution with minocycline, while the remainder experience at least 50% clearance of skin lesions.2 However, recurrence after stopping minocycline treatment is not uncommon. The mechanism by which minocycline works is unknown. Second-line treatment for those who cannot tolerate minocycline are macrolide antibiotics.6 Other treatment options with reported success include oral isotretinoin and topical retinoids, including tretinoin gel and tazarotene cream.3,7 Appropriate strength topical corticosteroids may be used for pruritus.

Allison Han

Ms. Han is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego, as well as the vice chair of the department of dermatology and a professor of dermatology and pediatrics at UC San Diego. They report having no conflicts of interest or financial disclosures. Email them at pdnews@frontlinemedcom.com.

Dr. Lawrence F. Eichenfield

References

1. Clin Cosmet Investig Dermatol. 2016 Aug 25;9:217-23.

2. Br J Dermatol. 2006 Feb;154(2):287-93.

3. Arch Dermatol. 2012 Apr;148(4):505-8.

4. J Am Acad Dermatol. 2003 Dec;49(6):1182-4.

5. Arch Dermatol. 2002 Feb;138(2):276-7.

6. J Am Acad Dermatol. 2001;44(4):652-5.

7. Am J Clin Dermatol. 2006;7(5):305-13.
 

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A 17-year-old male presents to the dermatology clinic for brown lesions on his central chest and back that have been present for about a year. The brown areas gradually have become scaly over time. They are asymptomatic. His pediatrician had given him hydrocortisone ointment to apply to the lesions, but there was no improvement. Review of systems was otherwise negative.

Dr. Lawrence F. Eichenfield
On examination, the patient is overweight. Hyperpigmented papules and plaques with mild scale are present on his central chest and back, converging toward the center of the chest and back and extending through the inframammary areas bilaterally. The papules and macules on the periphery of the involved skin create a net-like shape. The remainder of the physical examination is normal.

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CCSs have increased risk of hypertension

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CCSs have increased risk of hypertension

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Nurse checks patient’s blood pressure

A study of childhood cancer survivors (CCSs) suggests these individuals have an increased risk of developing hypertension as adults.

The CCSs studied had more than double the rate of hypertension observed in the matched general population.

Sex, age, race, and weight were all significantly associated with hypertension among CCSs, but most treatment types were not.

The exception was nephrectomy, which was associated with an increased risk of hypertension.

Todd M. Gibson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues conducted this research and reported the results in Cancer Epidemiology, Biomarkers & Prevention.

“High blood pressure is an important modifiable risk factor that increases the risk of heart problems in everyone,” Dr Gibson said. “Research has shown that high blood pressure can have an even greater negative impact on survivors of childhood cancer who were treated with cardiotoxic therapies such as anthracyclines or chest radiation.”

To assess the prevalence of hypertension among CCSs, Dr Gibson and his colleagues examined 3016 adults who were 10-year survivors of childhood cancers. The subjects were enrolled in the St. Jude Lifetime Cohort Study, which provides ongoing medical assessments of CCSs to advance knowledge of their long-term health outcomes.

The subjects’ mean age at the initial study assessment was 32, and 52% were male. Most (83%) were non-Hispanic white, 14% were non-Hispanic black, 2% were Hispanic, and 1% were “other.”

Thirty-seven percent of subjects had leukemia, 12% had Hodgkin lymphoma, and 7% had non-Hodgkin lymphoma.

Eighty-six percent of subjects had received chemotherapy, and 59% received radiation.

Results

Subjects were considered to have hypertension if their systolic blood pressure was 140 or greater, their diastolic blood pressure was 90 or greater, or if they had been previously diagnosed with hypertension and were taking antihypertensive medication.

The prevalence of hypertension was 2.6 times higher among CCSs than expected, based on age-, sex-, race- and body mass index-specific rates in the general population.

In addition, the incidence of hypertension increased for CCSs over time. Thirteen percent of CCSs had hypertension at age 30, 37% had it at age 40, and more than 70% had it at age 50.

Dr Gibson said rates of hypertension in CCSs matched rates in the general population of people about a decade older.

The researchers identified several factors that were significantly associated with hypertension among CCSs, including:

  • Male sex (odd ratio [OR], 1.38; 95% CI, 1.14–1.67)
  • Non-Hispanic black race (OR, 1.66; 95% CI, 1.28–2.16)
  • Older age at assessment (OR per 1 year of age, 1.10; 95% CI, 1.08–1.11)
  • Being overweight (OR, 1.58; 95% CI, 1.21–2.07)
  • Obesity (OR, 3.02; 95% CI, 2.34–3.88).

Exposure to any type of radiation or chemotherapy was not significantly associated with hypertension, but nephrectomy was (OR, 1.68; 95% CI, 1.11–2.53).

Dr Gibson said the lack of an association between hypertension and radiation/chemotherapy was surprising. It suggests the connection between childhood cancer survival and adult hypertension is multifactorial and worthy of future research.

In the meantime, he said, clinicians should be mindful that CCSs are more likely than the general public to develop hypertension.

“The good news is that, unlike prior cancer therapy, high blood pressure is a modifiable risk factor,” Dr Gibson noted. “Research is needed to identify effective interventions to prevent hypertension in survivors, but our results emphasize the importance of blood pressure surveillance and management.”

Dr Gibson said a limitation of this study is that it was based on blood pressure measurements taken at a single study visit. A clinical diagnosis of hypertension typically requires measurements taken at multiple intervals.

 

 

In addition, the St. Jude Lifetime Cohort is a group of CCSs who undergo frequent clinical follow-up, so its participants may have benefited from being monitored and may therefore be in better health than CCSs who have less comprehensive follow-up.

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Photo from NIH
Nurse checks patient’s blood pressure

A study of childhood cancer survivors (CCSs) suggests these individuals have an increased risk of developing hypertension as adults.

The CCSs studied had more than double the rate of hypertension observed in the matched general population.

Sex, age, race, and weight were all significantly associated with hypertension among CCSs, but most treatment types were not.

The exception was nephrectomy, which was associated with an increased risk of hypertension.

Todd M. Gibson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues conducted this research and reported the results in Cancer Epidemiology, Biomarkers & Prevention.

“High blood pressure is an important modifiable risk factor that increases the risk of heart problems in everyone,” Dr Gibson said. “Research has shown that high blood pressure can have an even greater negative impact on survivors of childhood cancer who were treated with cardiotoxic therapies such as anthracyclines or chest radiation.”

To assess the prevalence of hypertension among CCSs, Dr Gibson and his colleagues examined 3016 adults who were 10-year survivors of childhood cancers. The subjects were enrolled in the St. Jude Lifetime Cohort Study, which provides ongoing medical assessments of CCSs to advance knowledge of their long-term health outcomes.

The subjects’ mean age at the initial study assessment was 32, and 52% were male. Most (83%) were non-Hispanic white, 14% were non-Hispanic black, 2% were Hispanic, and 1% were “other.”

Thirty-seven percent of subjects had leukemia, 12% had Hodgkin lymphoma, and 7% had non-Hodgkin lymphoma.

Eighty-six percent of subjects had received chemotherapy, and 59% received radiation.

Results

Subjects were considered to have hypertension if their systolic blood pressure was 140 or greater, their diastolic blood pressure was 90 or greater, or if they had been previously diagnosed with hypertension and were taking antihypertensive medication.

The prevalence of hypertension was 2.6 times higher among CCSs than expected, based on age-, sex-, race- and body mass index-specific rates in the general population.

In addition, the incidence of hypertension increased for CCSs over time. Thirteen percent of CCSs had hypertension at age 30, 37% had it at age 40, and more than 70% had it at age 50.

Dr Gibson said rates of hypertension in CCSs matched rates in the general population of people about a decade older.

The researchers identified several factors that were significantly associated with hypertension among CCSs, including:

  • Male sex (odd ratio [OR], 1.38; 95% CI, 1.14–1.67)
  • Non-Hispanic black race (OR, 1.66; 95% CI, 1.28–2.16)
  • Older age at assessment (OR per 1 year of age, 1.10; 95% CI, 1.08–1.11)
  • Being overweight (OR, 1.58; 95% CI, 1.21–2.07)
  • Obesity (OR, 3.02; 95% CI, 2.34–3.88).

Exposure to any type of radiation or chemotherapy was not significantly associated with hypertension, but nephrectomy was (OR, 1.68; 95% CI, 1.11–2.53).

Dr Gibson said the lack of an association between hypertension and radiation/chemotherapy was surprising. It suggests the connection between childhood cancer survival and adult hypertension is multifactorial and worthy of future research.

In the meantime, he said, clinicians should be mindful that CCSs are more likely than the general public to develop hypertension.

“The good news is that, unlike prior cancer therapy, high blood pressure is a modifiable risk factor,” Dr Gibson noted. “Research is needed to identify effective interventions to prevent hypertension in survivors, but our results emphasize the importance of blood pressure surveillance and management.”

Dr Gibson said a limitation of this study is that it was based on blood pressure measurements taken at a single study visit. A clinical diagnosis of hypertension typically requires measurements taken at multiple intervals.

 

 

In addition, the St. Jude Lifetime Cohort is a group of CCSs who undergo frequent clinical follow-up, so its participants may have benefited from being monitored and may therefore be in better health than CCSs who have less comprehensive follow-up.

Photo from NIH
Nurse checks patient’s blood pressure

A study of childhood cancer survivors (CCSs) suggests these individuals have an increased risk of developing hypertension as adults.

The CCSs studied had more than double the rate of hypertension observed in the matched general population.

Sex, age, race, and weight were all significantly associated with hypertension among CCSs, but most treatment types were not.

The exception was nephrectomy, which was associated with an increased risk of hypertension.

Todd M. Gibson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues conducted this research and reported the results in Cancer Epidemiology, Biomarkers & Prevention.

“High blood pressure is an important modifiable risk factor that increases the risk of heart problems in everyone,” Dr Gibson said. “Research has shown that high blood pressure can have an even greater negative impact on survivors of childhood cancer who were treated with cardiotoxic therapies such as anthracyclines or chest radiation.”

To assess the prevalence of hypertension among CCSs, Dr Gibson and his colleagues examined 3016 adults who were 10-year survivors of childhood cancers. The subjects were enrolled in the St. Jude Lifetime Cohort Study, which provides ongoing medical assessments of CCSs to advance knowledge of their long-term health outcomes.

The subjects’ mean age at the initial study assessment was 32, and 52% were male. Most (83%) were non-Hispanic white, 14% were non-Hispanic black, 2% were Hispanic, and 1% were “other.”

Thirty-seven percent of subjects had leukemia, 12% had Hodgkin lymphoma, and 7% had non-Hodgkin lymphoma.

Eighty-six percent of subjects had received chemotherapy, and 59% received radiation.

Results

Subjects were considered to have hypertension if their systolic blood pressure was 140 or greater, their diastolic blood pressure was 90 or greater, or if they had been previously diagnosed with hypertension and were taking antihypertensive medication.

The prevalence of hypertension was 2.6 times higher among CCSs than expected, based on age-, sex-, race- and body mass index-specific rates in the general population.

In addition, the incidence of hypertension increased for CCSs over time. Thirteen percent of CCSs had hypertension at age 30, 37% had it at age 40, and more than 70% had it at age 50.

Dr Gibson said rates of hypertension in CCSs matched rates in the general population of people about a decade older.

The researchers identified several factors that were significantly associated with hypertension among CCSs, including:

  • Male sex (odd ratio [OR], 1.38; 95% CI, 1.14–1.67)
  • Non-Hispanic black race (OR, 1.66; 95% CI, 1.28–2.16)
  • Older age at assessment (OR per 1 year of age, 1.10; 95% CI, 1.08–1.11)
  • Being overweight (OR, 1.58; 95% CI, 1.21–2.07)
  • Obesity (OR, 3.02; 95% CI, 2.34–3.88).

Exposure to any type of radiation or chemotherapy was not significantly associated with hypertension, but nephrectomy was (OR, 1.68; 95% CI, 1.11–2.53).

Dr Gibson said the lack of an association between hypertension and radiation/chemotherapy was surprising. It suggests the connection between childhood cancer survival and adult hypertension is multifactorial and worthy of future research.

In the meantime, he said, clinicians should be mindful that CCSs are more likely than the general public to develop hypertension.

“The good news is that, unlike prior cancer therapy, high blood pressure is a modifiable risk factor,” Dr Gibson noted. “Research is needed to identify effective interventions to prevent hypertension in survivors, but our results emphasize the importance of blood pressure surveillance and management.”

Dr Gibson said a limitation of this study is that it was based on blood pressure measurements taken at a single study visit. A clinical diagnosis of hypertension typically requires measurements taken at multiple intervals.

 

 

In addition, the St. Jude Lifetime Cohort is a group of CCSs who undergo frequent clinical follow-up, so its participants may have benefited from being monitored and may therefore be in better health than CCSs who have less comprehensive follow-up.

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Preventing substance use

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Substance use disorders are affecting every pediatric practice as they are major contributors to morbidity and mortality in young people. With the ongoing risks of binge drinking, the current epidemic of opioid addiction and overdose deaths in the United States, and the shifting legal status and public perception of the risk of marijuana, how to deal with substance use disorders seems to be the focus of public conversation these days. Some of the most effective and cost-effective interventions for substance abuse disorders are preventive ones, such as parent education and early recognition in pediatric practice.

Substance abuse risk

rez-art/Thinkstock
While the prevalence of substance use disorders has dropped in youth since the 1980s, an estimated 5% of youth aged 12-17 years suffered from a substance use disorder in 2014, according to the Substance Abuse and Mental Health Services Administration (SAMHSA). Epidemiologic studies have repeatedly demonstrated that earlier first use of alcohol (under 14 years old) or tobacco predicts use of illicit drugs and is associated with higher lifetime rates of alcohol and drug dependence. There is emerging evidence that early use of addictive substances such as tobacco and alcohol has distinct neurobiologic effects that increase the propensity toward dependence, rather than being simply a function of an underlying vulnerability to dependence.1 While tobacco and alcohol use among youth have been trending down since the 1980s, rates are still high. The 2016 Monitoring the Future Survey found that 7% of 8th graders, 20% of 10th graders, and 33% of 12th graders reported having used alcohol in the 30 days prior to the study. Of particular concern is the recent upward trend in rates of binge drinking (five or more drinks in 2 hours), particularly among those enrolled in college, with rates as high as 43% in 2014, according to SAMHSA. Also notable is the strong shift in attitudes of youth toward marijuana, with fewer believing that “regular use” poses risks. Finally, rates of prescription opioid abuse among youth have started to decline, from more than 11% of 12th graders in 2013 to less than 8% in 2016. But there is evidence that those who regularly use marijuana in adolescence are more likely to abuse prescription opioids in their 20s. So interventions that can delay the first use of any substance, and discourage use of particularly addictive substances, can be a very effective way of preventing later substance use disorders.

We cannot yet predict who can safely “experiment” with substances or who will develop dependency. However, there is information that we can use to identify those at greater risk. Youth who have a first-degree relative with a substance use disorder are at greater risk for developing such a disorder themselves, and this is especially so if there is a family history of alcoholism. Youth who suffer from a psychiatric illness, particularly from anxiety and mood disorders, have a special vulnerability to abusing substances, particularly when their underlying illness is untreated or incompletely treated. Youth with ADHD are at substantially elevated risk of developing substance use disorders, although there is a complex relationship between these two problems. The evidence currently suggests that for youth who began effective treatment prior to puberty, there is no elevation in risk, but for those who did not, there is a substantially elevated risk of substance use disorders. Finally, there has been research that indicates that children with a combination of sensation-seeking, high impulsivity, anxiety-sensitivity, and hopelessness are at the highest risk for substance use disorders.2
 

Prevention efforts you can make: To your patients

The first step in your prevention efforts is an open conversation about drugs and alcohol. Ask your middle schoolers about whether they have tried alcohol or any drugs. Have their friends? What are kids saying about alcohol? About marijuana? Vaping? Are there other substances that kids are talking about or trying? Be genuinely curious, warm, and nonjudgmental. Find out what they think the risks of these substances may be. If appropriate, offer them some education about known risks of substances to the developing brain, to school or athletic performance, and so on. You can teach them about other trusted resources, such as the National Institute on Drug Abuse (NIDA), which has a resource specifically for teens (teens.drugabuse.gov).

Dr. Susan D. Swick
Be pragmatic. After learning about what is being used by their peers, think with them about how they could say no to trying a drink, a smoke, or something more without creating drama or drawing attention to themselves. Are they seeing worrisome problems at parties, or are their friends using substances? What should they do if they see a friend falling unconscious? Have they seen anyone in a dangerous situation? How do they handle driving? If an anxious or impulsive adolescent has a plan to respond in these situations, they are much more likely to follow their plan to delay or decline.

For your high school students and those heading off to college, provide a safe place to talk about what they have tried and whether they (or you) have any worries about substance use. You have a unique combination of clinical authority and expertise in them as individuals, and can help them meaningfully plan how to handle their choices. You might talk about the specific risks of binge drinking, from sexual assault to alcohol poisoning and permanent cognitive effects on their developing brains. They also can benefit from hearing about the actual risks of frequent marijuana use, including impaired cognitive performance (and permanent IQ decline), and ongoing risks to their still-developing brains. Don’t be surprised if your older adolescent patients want to educate you about risks. Be curious and humble, and don’t be afraid to go together to a third party for information. You should encourage their efforts to think critically, and be empathic to their dilemma as they try to balance risks against their drive to have new experiences, to be independent, and to be strongly connected to their peers.

Adolescents should hear about your concern about their specific risks with drugs and alcohol, such as a history of traumatic brain injury (concussion), a family history of drug or alcohol dependence, or their own diagnosis of anxiety, depression, or ADHD. You might point out that because they have not tried any drugs or alcohol in high school, they may be prone to having too much to drink when they first try it. Or you might observe that because they have an anxiety disorder, they are vulnerable to becoming dependent on alcohol. Hearing about their specific level of risk equips them to make wiser choices in the context of their growing autonomy.
 
 

 

Prevention efforts you can make: To the parents

Your other prevention strategies should include parents. Studies have shown that when parents have clear rules and expectations about drug and alcohol use, and are consistent about enforcing consequences in their home, their children are significantly less likely than their peers to have experimented with drugs or alcohol by their senior year in high school. Parents of children headed to middle school should hear about this fact, alongside accurate information about the risks associated with alcohol and specific drugs for the developing brain.

Dr. Michael S. Jellinek
Parents also benefit from practical strategies on how to talk about drugs and alcohol with their children. Letting parents know that 5th or 6th grade is not too early to have a conversation in which they introduce their rules around drugs and alcohol. Parents should look for opportunities to talk often with their kids in less proscriptive ways about drugs and alcohol. Such opportunities can arise around stories in the news about sports stars, musicians, or television stars and drug or alcohol use. Or they may occur when watching a favorite television show or movie together. Talking about these issues in a less confrontational way, when the subject is a celebrity or character rather than your child, can make the conversation more open, comfortable, and useful for everyone.

Finally, parents need to hear that they can be effective disciplinarians, while also making clear to their children that safety comes first, and that their rules should have clear exceptions for safety. If the parents have a rule against any use of alcohol or drugs, there should be an exception if their child is out and feels unsafe. If they are drunk, or their driver has been drinking, they can call for a ride and will not be in (much) trouble. Rules don’t have to be draconian to be effective; they should always support honesty and safety first. This is a lot of territory to cover, and you do not have to be the only resource for parents. Reliable online resources, such as NIDA’s and SAMHSA’s websites, are full of useful information, and others, such as teen-safe.org, have detailed resources for parents in particular.
 

References

1. Hum Genet. 2012 Jun;131(6):779-89.

2. Alcohol Clin Exp Res. 2013 Jan;37(Suppl 1):E281-90.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

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Substance use disorders are affecting every pediatric practice as they are major contributors to morbidity and mortality in young people. With the ongoing risks of binge drinking, the current epidemic of opioid addiction and overdose deaths in the United States, and the shifting legal status and public perception of the risk of marijuana, how to deal with substance use disorders seems to be the focus of public conversation these days. Some of the most effective and cost-effective interventions for substance abuse disorders are preventive ones, such as parent education and early recognition in pediatric practice.

Substance abuse risk

rez-art/Thinkstock
While the prevalence of substance use disorders has dropped in youth since the 1980s, an estimated 5% of youth aged 12-17 years suffered from a substance use disorder in 2014, according to the Substance Abuse and Mental Health Services Administration (SAMHSA). Epidemiologic studies have repeatedly demonstrated that earlier first use of alcohol (under 14 years old) or tobacco predicts use of illicit drugs and is associated with higher lifetime rates of alcohol and drug dependence. There is emerging evidence that early use of addictive substances such as tobacco and alcohol has distinct neurobiologic effects that increase the propensity toward dependence, rather than being simply a function of an underlying vulnerability to dependence.1 While tobacco and alcohol use among youth have been trending down since the 1980s, rates are still high. The 2016 Monitoring the Future Survey found that 7% of 8th graders, 20% of 10th graders, and 33% of 12th graders reported having used alcohol in the 30 days prior to the study. Of particular concern is the recent upward trend in rates of binge drinking (five or more drinks in 2 hours), particularly among those enrolled in college, with rates as high as 43% in 2014, according to SAMHSA. Also notable is the strong shift in attitudes of youth toward marijuana, with fewer believing that “regular use” poses risks. Finally, rates of prescription opioid abuse among youth have started to decline, from more than 11% of 12th graders in 2013 to less than 8% in 2016. But there is evidence that those who regularly use marijuana in adolescence are more likely to abuse prescription opioids in their 20s. So interventions that can delay the first use of any substance, and discourage use of particularly addictive substances, can be a very effective way of preventing later substance use disorders.

We cannot yet predict who can safely “experiment” with substances or who will develop dependency. However, there is information that we can use to identify those at greater risk. Youth who have a first-degree relative with a substance use disorder are at greater risk for developing such a disorder themselves, and this is especially so if there is a family history of alcoholism. Youth who suffer from a psychiatric illness, particularly from anxiety and mood disorders, have a special vulnerability to abusing substances, particularly when their underlying illness is untreated or incompletely treated. Youth with ADHD are at substantially elevated risk of developing substance use disorders, although there is a complex relationship between these two problems. The evidence currently suggests that for youth who began effective treatment prior to puberty, there is no elevation in risk, but for those who did not, there is a substantially elevated risk of substance use disorders. Finally, there has been research that indicates that children with a combination of sensation-seeking, high impulsivity, anxiety-sensitivity, and hopelessness are at the highest risk for substance use disorders.2
 

Prevention efforts you can make: To your patients

The first step in your prevention efforts is an open conversation about drugs and alcohol. Ask your middle schoolers about whether they have tried alcohol or any drugs. Have their friends? What are kids saying about alcohol? About marijuana? Vaping? Are there other substances that kids are talking about or trying? Be genuinely curious, warm, and nonjudgmental. Find out what they think the risks of these substances may be. If appropriate, offer them some education about known risks of substances to the developing brain, to school or athletic performance, and so on. You can teach them about other trusted resources, such as the National Institute on Drug Abuse (NIDA), which has a resource specifically for teens (teens.drugabuse.gov).

Dr. Susan D. Swick
Be pragmatic. After learning about what is being used by their peers, think with them about how they could say no to trying a drink, a smoke, or something more without creating drama or drawing attention to themselves. Are they seeing worrisome problems at parties, or are their friends using substances? What should they do if they see a friend falling unconscious? Have they seen anyone in a dangerous situation? How do they handle driving? If an anxious or impulsive adolescent has a plan to respond in these situations, they are much more likely to follow their plan to delay or decline.

For your high school students and those heading off to college, provide a safe place to talk about what they have tried and whether they (or you) have any worries about substance use. You have a unique combination of clinical authority and expertise in them as individuals, and can help them meaningfully plan how to handle their choices. You might talk about the specific risks of binge drinking, from sexual assault to alcohol poisoning and permanent cognitive effects on their developing brains. They also can benefit from hearing about the actual risks of frequent marijuana use, including impaired cognitive performance (and permanent IQ decline), and ongoing risks to their still-developing brains. Don’t be surprised if your older adolescent patients want to educate you about risks. Be curious and humble, and don’t be afraid to go together to a third party for information. You should encourage their efforts to think critically, and be empathic to their dilemma as they try to balance risks against their drive to have new experiences, to be independent, and to be strongly connected to their peers.

Adolescents should hear about your concern about their specific risks with drugs and alcohol, such as a history of traumatic brain injury (concussion), a family history of drug or alcohol dependence, or their own diagnosis of anxiety, depression, or ADHD. You might point out that because they have not tried any drugs or alcohol in high school, they may be prone to having too much to drink when they first try it. Or you might observe that because they have an anxiety disorder, they are vulnerable to becoming dependent on alcohol. Hearing about their specific level of risk equips them to make wiser choices in the context of their growing autonomy.
 
 

 

Prevention efforts you can make: To the parents

Your other prevention strategies should include parents. Studies have shown that when parents have clear rules and expectations about drug and alcohol use, and are consistent about enforcing consequences in their home, their children are significantly less likely than their peers to have experimented with drugs or alcohol by their senior year in high school. Parents of children headed to middle school should hear about this fact, alongside accurate information about the risks associated with alcohol and specific drugs for the developing brain.

Dr. Michael S. Jellinek
Parents also benefit from practical strategies on how to talk about drugs and alcohol with their children. Letting parents know that 5th or 6th grade is not too early to have a conversation in which they introduce their rules around drugs and alcohol. Parents should look for opportunities to talk often with their kids in less proscriptive ways about drugs and alcohol. Such opportunities can arise around stories in the news about sports stars, musicians, or television stars and drug or alcohol use. Or they may occur when watching a favorite television show or movie together. Talking about these issues in a less confrontational way, when the subject is a celebrity or character rather than your child, can make the conversation more open, comfortable, and useful for everyone.

Finally, parents need to hear that they can be effective disciplinarians, while also making clear to their children that safety comes first, and that their rules should have clear exceptions for safety. If the parents have a rule against any use of alcohol or drugs, there should be an exception if their child is out and feels unsafe. If they are drunk, or their driver has been drinking, they can call for a ride and will not be in (much) trouble. Rules don’t have to be draconian to be effective; they should always support honesty and safety first. This is a lot of territory to cover, and you do not have to be the only resource for parents. Reliable online resources, such as NIDA’s and SAMHSA’s websites, are full of useful information, and others, such as teen-safe.org, have detailed resources for parents in particular.
 

References

1. Hum Genet. 2012 Jun;131(6):779-89.

2. Alcohol Clin Exp Res. 2013 Jan;37(Suppl 1):E281-90.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

Substance use disorders are affecting every pediatric practice as they are major contributors to morbidity and mortality in young people. With the ongoing risks of binge drinking, the current epidemic of opioid addiction and overdose deaths in the United States, and the shifting legal status and public perception of the risk of marijuana, how to deal with substance use disorders seems to be the focus of public conversation these days. Some of the most effective and cost-effective interventions for substance abuse disorders are preventive ones, such as parent education and early recognition in pediatric practice.

Substance abuse risk

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While the prevalence of substance use disorders has dropped in youth since the 1980s, an estimated 5% of youth aged 12-17 years suffered from a substance use disorder in 2014, according to the Substance Abuse and Mental Health Services Administration (SAMHSA). Epidemiologic studies have repeatedly demonstrated that earlier first use of alcohol (under 14 years old) or tobacco predicts use of illicit drugs and is associated with higher lifetime rates of alcohol and drug dependence. There is emerging evidence that early use of addictive substances such as tobacco and alcohol has distinct neurobiologic effects that increase the propensity toward dependence, rather than being simply a function of an underlying vulnerability to dependence.1 While tobacco and alcohol use among youth have been trending down since the 1980s, rates are still high. The 2016 Monitoring the Future Survey found that 7% of 8th graders, 20% of 10th graders, and 33% of 12th graders reported having used alcohol in the 30 days prior to the study. Of particular concern is the recent upward trend in rates of binge drinking (five or more drinks in 2 hours), particularly among those enrolled in college, with rates as high as 43% in 2014, according to SAMHSA. Also notable is the strong shift in attitudes of youth toward marijuana, with fewer believing that “regular use” poses risks. Finally, rates of prescription opioid abuse among youth have started to decline, from more than 11% of 12th graders in 2013 to less than 8% in 2016. But there is evidence that those who regularly use marijuana in adolescence are more likely to abuse prescription opioids in their 20s. So interventions that can delay the first use of any substance, and discourage use of particularly addictive substances, can be a very effective way of preventing later substance use disorders.

We cannot yet predict who can safely “experiment” with substances or who will develop dependency. However, there is information that we can use to identify those at greater risk. Youth who have a first-degree relative with a substance use disorder are at greater risk for developing such a disorder themselves, and this is especially so if there is a family history of alcoholism. Youth who suffer from a psychiatric illness, particularly from anxiety and mood disorders, have a special vulnerability to abusing substances, particularly when their underlying illness is untreated or incompletely treated. Youth with ADHD are at substantially elevated risk of developing substance use disorders, although there is a complex relationship between these two problems. The evidence currently suggests that for youth who began effective treatment prior to puberty, there is no elevation in risk, but for those who did not, there is a substantially elevated risk of substance use disorders. Finally, there has been research that indicates that children with a combination of sensation-seeking, high impulsivity, anxiety-sensitivity, and hopelessness are at the highest risk for substance use disorders.2
 

Prevention efforts you can make: To your patients

The first step in your prevention efforts is an open conversation about drugs and alcohol. Ask your middle schoolers about whether they have tried alcohol or any drugs. Have their friends? What are kids saying about alcohol? About marijuana? Vaping? Are there other substances that kids are talking about or trying? Be genuinely curious, warm, and nonjudgmental. Find out what they think the risks of these substances may be. If appropriate, offer them some education about known risks of substances to the developing brain, to school or athletic performance, and so on. You can teach them about other trusted resources, such as the National Institute on Drug Abuse (NIDA), which has a resource specifically for teens (teens.drugabuse.gov).

Dr. Susan D. Swick
Be pragmatic. After learning about what is being used by their peers, think with them about how they could say no to trying a drink, a smoke, or something more without creating drama or drawing attention to themselves. Are they seeing worrisome problems at parties, or are their friends using substances? What should they do if they see a friend falling unconscious? Have they seen anyone in a dangerous situation? How do they handle driving? If an anxious or impulsive adolescent has a plan to respond in these situations, they are much more likely to follow their plan to delay or decline.

For your high school students and those heading off to college, provide a safe place to talk about what they have tried and whether they (or you) have any worries about substance use. You have a unique combination of clinical authority and expertise in them as individuals, and can help them meaningfully plan how to handle their choices. You might talk about the specific risks of binge drinking, from sexual assault to alcohol poisoning and permanent cognitive effects on their developing brains. They also can benefit from hearing about the actual risks of frequent marijuana use, including impaired cognitive performance (and permanent IQ decline), and ongoing risks to their still-developing brains. Don’t be surprised if your older adolescent patients want to educate you about risks. Be curious and humble, and don’t be afraid to go together to a third party for information. You should encourage their efforts to think critically, and be empathic to their dilemma as they try to balance risks against their drive to have new experiences, to be independent, and to be strongly connected to their peers.

Adolescents should hear about your concern about their specific risks with drugs and alcohol, such as a history of traumatic brain injury (concussion), a family history of drug or alcohol dependence, or their own diagnosis of anxiety, depression, or ADHD. You might point out that because they have not tried any drugs or alcohol in high school, they may be prone to having too much to drink when they first try it. Or you might observe that because they have an anxiety disorder, they are vulnerable to becoming dependent on alcohol. Hearing about their specific level of risk equips them to make wiser choices in the context of their growing autonomy.
 
 

 

Prevention efforts you can make: To the parents

Your other prevention strategies should include parents. Studies have shown that when parents have clear rules and expectations about drug and alcohol use, and are consistent about enforcing consequences in their home, their children are significantly less likely than their peers to have experimented with drugs or alcohol by their senior year in high school. Parents of children headed to middle school should hear about this fact, alongside accurate information about the risks associated with alcohol and specific drugs for the developing brain.

Dr. Michael S. Jellinek
Parents also benefit from practical strategies on how to talk about drugs and alcohol with their children. Letting parents know that 5th or 6th grade is not too early to have a conversation in which they introduce their rules around drugs and alcohol. Parents should look for opportunities to talk often with their kids in less proscriptive ways about drugs and alcohol. Such opportunities can arise around stories in the news about sports stars, musicians, or television stars and drug or alcohol use. Or they may occur when watching a favorite television show or movie together. Talking about these issues in a less confrontational way, when the subject is a celebrity or character rather than your child, can make the conversation more open, comfortable, and useful for everyone.

Finally, parents need to hear that they can be effective disciplinarians, while also making clear to their children that safety comes first, and that their rules should have clear exceptions for safety. If the parents have a rule against any use of alcohol or drugs, there should be an exception if their child is out and feels unsafe. If they are drunk, or their driver has been drinking, they can call for a ride and will not be in (much) trouble. Rules don’t have to be draconian to be effective; they should always support honesty and safety first. This is a lot of territory to cover, and you do not have to be the only resource for parents. Reliable online resources, such as NIDA’s and SAMHSA’s websites, are full of useful information, and others, such as teen-safe.org, have detailed resources for parents in particular.
 

References

1. Hum Genet. 2012 Jun;131(6):779-89.

2. Alcohol Clin Exp Res. 2013 Jan;37(Suppl 1):E281-90.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

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Journal of Hospital Medicine – Nov. 2017

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Sustainability in the AAP Bronchiolitis Quality Improvement Project

 

BACKGROUND AND OBJECTIVES: Adherence to American Academy of Pediatrics (AAP) bronchiolitis clinical practice guideline recommendations improved significantly through the AAP’s multi-institutional collaborative the Bronchiolitis Quality Improvement Project (BQIP). We assessed sustainability of improvements at participating institutions for 1 year following completion of the collaborative.

METHODS: Twenty-one multidisciplinary hospital-based teams provided monthly data for key inpatient bronchiolitis measures during baseline and intervention bronchiolitis seasons. Nine sites provided data in the season following completion of the collaborative. Encounters included children younger than 24 months who were hospitalized for bronchiolitis without comorbid chronic illness, prematurity, or intensive care. Changes between baseline-, intervention-, and sustainability-season data were assessed using generalized linear mixed-effects models with site-specific random effects. Differences between hospital characteristics, baseline performance, and initial improvement among sites that did and did not participate in the sustainability season were compared.

RESULTS: A total of 2,275 discharges were reviewed, comprising 995 baseline, 877 intervention, and 403 sustainability-season encounters. Improvements in all key bronchiolitis quality measures achieved during the intervention season were maintained during the sustainability season, and orders for intermittent pulse oximetry increased from 40.6% (95% confidence interval, 22.8-61.1) to 79.2% (95% CI, 58.0-91.3). Sites that did and did not participate in the sustainability season had similar characteristics.

DISCUSSION: BQIP participating sites maintained improvements in key bronchiolitis quality measures for 1 year following the project’s completion. This approach, which provided an evidence-based best-practice toolkit while building the quality-improvement capacity of local interdisciplinary teams, may support performance gains that persist beyond the active phase of the collaborative.
 

Also in JHM this month

The effect of an inpatient smoking cessation treatment program on hospital readmissions and length of stayAUTHORS: Eline M. van den Broek-Altenburg, MS, MA, Adam J. Atherly, PhD

Treatment trends and outcomes in healthcare-associated pneumoniaAUTHORS: Sarah Haessler, MD; Tara Lagu, MD, MPH; Peter K. Lindenauer, MD, MSc; Daniel J. Skiest, MD; Aruna Priya, MA, MSc; Penelope S. Pekow, PhD; Marya D. Zilberberg, MD, MPH; Thomas L. Higgins, MD, MBA; Michael B. Rothberg, MD, MPH

What’s the purpose of rounds? A qualitative study examining the perceptions of faculty and studentsAUTHORS: Oliver Hulland; Jeanne Farnan, MD, MHPE; Raphael Rabinowitz; Lisa Kearns, MD, MS; Michele Long, MD; Bradley Monash, MD; Priti Bhansali, MD; H. Barrett Fromme, MD, MHPE

Association between anemia and fatigue in hospitalized patients: does the measure of anemia matter?AUTHORS: Micah T. Prochaska, MD, MS; Richard Newcomb, BA; Graham Block, BA; Brian Park, BA; David O. Meltzer MD, PhD

Helping seniors plan for posthospital discharge needs before a hospitalization occurs: Results from the randomized control trial of planyourlifespan.orgAUTHORS: Lee A. Lindquist, MD, MPH, MBA; Vanessa Ramirez-Zohfeld, MPH; Priya D. Sunkara, MA; Chris Forcucci, RN, BSN; Dianne S. Campbell, BS; Phyllis Mitzen, MA; Jody D. Ciolino, PhD; Gayle Kricke, MSW; Anne Seltzer, LSW; Ana V. Ramirez, BA; Kenzie A. Cameron, PhD, MPH

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Sustainability in the AAP Bronchiolitis Quality Improvement Project
Sustainability in the AAP Bronchiolitis Quality Improvement Project

 

BACKGROUND AND OBJECTIVES: Adherence to American Academy of Pediatrics (AAP) bronchiolitis clinical practice guideline recommendations improved significantly through the AAP’s multi-institutional collaborative the Bronchiolitis Quality Improvement Project (BQIP). We assessed sustainability of improvements at participating institutions for 1 year following completion of the collaborative.

METHODS: Twenty-one multidisciplinary hospital-based teams provided monthly data for key inpatient bronchiolitis measures during baseline and intervention bronchiolitis seasons. Nine sites provided data in the season following completion of the collaborative. Encounters included children younger than 24 months who were hospitalized for bronchiolitis without comorbid chronic illness, prematurity, or intensive care. Changes between baseline-, intervention-, and sustainability-season data were assessed using generalized linear mixed-effects models with site-specific random effects. Differences between hospital characteristics, baseline performance, and initial improvement among sites that did and did not participate in the sustainability season were compared.

RESULTS: A total of 2,275 discharges were reviewed, comprising 995 baseline, 877 intervention, and 403 sustainability-season encounters. Improvements in all key bronchiolitis quality measures achieved during the intervention season were maintained during the sustainability season, and orders for intermittent pulse oximetry increased from 40.6% (95% confidence interval, 22.8-61.1) to 79.2% (95% CI, 58.0-91.3). Sites that did and did not participate in the sustainability season had similar characteristics.

DISCUSSION: BQIP participating sites maintained improvements in key bronchiolitis quality measures for 1 year following the project’s completion. This approach, which provided an evidence-based best-practice toolkit while building the quality-improvement capacity of local interdisciplinary teams, may support performance gains that persist beyond the active phase of the collaborative.
 

Also in JHM this month

The effect of an inpatient smoking cessation treatment program on hospital readmissions and length of stayAUTHORS: Eline M. van den Broek-Altenburg, MS, MA, Adam J. Atherly, PhD

Treatment trends and outcomes in healthcare-associated pneumoniaAUTHORS: Sarah Haessler, MD; Tara Lagu, MD, MPH; Peter K. Lindenauer, MD, MSc; Daniel J. Skiest, MD; Aruna Priya, MA, MSc; Penelope S. Pekow, PhD; Marya D. Zilberberg, MD, MPH; Thomas L. Higgins, MD, MBA; Michael B. Rothberg, MD, MPH

What’s the purpose of rounds? A qualitative study examining the perceptions of faculty and studentsAUTHORS: Oliver Hulland; Jeanne Farnan, MD, MHPE; Raphael Rabinowitz; Lisa Kearns, MD, MS; Michele Long, MD; Bradley Monash, MD; Priti Bhansali, MD; H. Barrett Fromme, MD, MHPE

Association between anemia and fatigue in hospitalized patients: does the measure of anemia matter?AUTHORS: Micah T. Prochaska, MD, MS; Richard Newcomb, BA; Graham Block, BA; Brian Park, BA; David O. Meltzer MD, PhD

Helping seniors plan for posthospital discharge needs before a hospitalization occurs: Results from the randomized control trial of planyourlifespan.orgAUTHORS: Lee A. Lindquist, MD, MPH, MBA; Vanessa Ramirez-Zohfeld, MPH; Priya D. Sunkara, MA; Chris Forcucci, RN, BSN; Dianne S. Campbell, BS; Phyllis Mitzen, MA; Jody D. Ciolino, PhD; Gayle Kricke, MSW; Anne Seltzer, LSW; Ana V. Ramirez, BA; Kenzie A. Cameron, PhD, MPH

 

BACKGROUND AND OBJECTIVES: Adherence to American Academy of Pediatrics (AAP) bronchiolitis clinical practice guideline recommendations improved significantly through the AAP’s multi-institutional collaborative the Bronchiolitis Quality Improvement Project (BQIP). We assessed sustainability of improvements at participating institutions for 1 year following completion of the collaborative.

METHODS: Twenty-one multidisciplinary hospital-based teams provided monthly data for key inpatient bronchiolitis measures during baseline and intervention bronchiolitis seasons. Nine sites provided data in the season following completion of the collaborative. Encounters included children younger than 24 months who were hospitalized for bronchiolitis without comorbid chronic illness, prematurity, or intensive care. Changes between baseline-, intervention-, and sustainability-season data were assessed using generalized linear mixed-effects models with site-specific random effects. Differences between hospital characteristics, baseline performance, and initial improvement among sites that did and did not participate in the sustainability season were compared.

RESULTS: A total of 2,275 discharges were reviewed, comprising 995 baseline, 877 intervention, and 403 sustainability-season encounters. Improvements in all key bronchiolitis quality measures achieved during the intervention season were maintained during the sustainability season, and orders for intermittent pulse oximetry increased from 40.6% (95% confidence interval, 22.8-61.1) to 79.2% (95% CI, 58.0-91.3). Sites that did and did not participate in the sustainability season had similar characteristics.

DISCUSSION: BQIP participating sites maintained improvements in key bronchiolitis quality measures for 1 year following the project’s completion. This approach, which provided an evidence-based best-practice toolkit while building the quality-improvement capacity of local interdisciplinary teams, may support performance gains that persist beyond the active phase of the collaborative.
 

Also in JHM this month

The effect of an inpatient smoking cessation treatment program on hospital readmissions and length of stayAUTHORS: Eline M. van den Broek-Altenburg, MS, MA, Adam J. Atherly, PhD

Treatment trends and outcomes in healthcare-associated pneumoniaAUTHORS: Sarah Haessler, MD; Tara Lagu, MD, MPH; Peter K. Lindenauer, MD, MSc; Daniel J. Skiest, MD; Aruna Priya, MA, MSc; Penelope S. Pekow, PhD; Marya D. Zilberberg, MD, MPH; Thomas L. Higgins, MD, MBA; Michael B. Rothberg, MD, MPH

What’s the purpose of rounds? A qualitative study examining the perceptions of faculty and studentsAUTHORS: Oliver Hulland; Jeanne Farnan, MD, MHPE; Raphael Rabinowitz; Lisa Kearns, MD, MS; Michele Long, MD; Bradley Monash, MD; Priti Bhansali, MD; H. Barrett Fromme, MD, MHPE

Association between anemia and fatigue in hospitalized patients: does the measure of anemia matter?AUTHORS: Micah T. Prochaska, MD, MS; Richard Newcomb, BA; Graham Block, BA; Brian Park, BA; David O. Meltzer MD, PhD

Helping seniors plan for posthospital discharge needs before a hospitalization occurs: Results from the randomized control trial of planyourlifespan.orgAUTHORS: Lee A. Lindquist, MD, MPH, MBA; Vanessa Ramirez-Zohfeld, MPH; Priya D. Sunkara, MA; Chris Forcucci, RN, BSN; Dianne S. Campbell, BS; Phyllis Mitzen, MA; Jody D. Ciolino, PhD; Gayle Kricke, MSW; Anne Seltzer, LSW; Ana V. Ramirez, BA; Kenzie A. Cameron, PhD, MPH

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Screening for postpartum depression is essential

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CHICAGO – Screening mothers for postpartum depression is critical, because of the potential negative consequences for the child, according to Nerissa S. Bauer, MD, MPH.

Postpartum depression is the best known mood disorder related to pregnancy, but it’s not the only one. Perinatal mood and anxiety disorders exist along a spectrum, she told attendees at the American Academy of Pediatrics annual meeting. That spectrum includes prenatal depression, prenatal anxiety, “baby blues,” postpartum depression, posttraumatic stress disorder (PSTD), and postpartum anxiety with panic attacks and/or obsessive-compulsive disorder (OCD).

monkeybusinessimages/Thinkstock
Baby blues in mothers after delivery – temporary, mild symptoms of depression that don’t interfere with caring for the baby and aren’t cause for alarm – are a normal occurrence and have been reported worldwide. About 50%-80% of women experience baby blues. These symptoms tend to peak around 5 days post partum. “Pediatricians can provide reassurance, emotional support, and demystification” in helping women cope with baby blues, said Dr. Bauer, a pediatrician at Indiana University, Indianapolis.



Postpartum mood disorders

Postpartum depression (PPD), however, is serious and requires intervention. An estimated 10%-20% of new mothers experience PPD, but the numbers are much higher in at-risk communities. Up to 48% of mothers in low-income households and 40%-60% of adolescent mothers in low-income households experience it. Yet only about 15% of these higher-risk women seek treatment for PPD (Pediatrics. 2010 Nov;126[5]:1032-9).

PPD symptoms are similar to the usual symptoms of a depressive disorder: depressed mood, irritability, changes in sleep and/or appetite, fatigue, sleepiness, loss of interest in activities, inability to feel pleasure in everyday life, guilt, difficulty concentrating, indecisiveness, low energy, despair, and feelings of worthlessness. The biggest difference – and most important symptom – is that women with PPD may have thoughts about harming not only themselves but also their child. This symptom calls for immediate intervention and sometimes can be a sign of postpartum psychosis.

Postpartum psychosis is rare, occurring in about 1-3 out of 1,000 women, but its seriousness requires immediate medical attention, including hospitalization in most cases. The best established risk factor is preexisting bipolar disorder. Postpartum psychosis usually occurs in the first 4 weeks after delivery, with symptoms that include paranoia, severe mood shifts, hallucinations, delusions, and suicidal and/or homicidal thoughts.

Fathers also can experience depression after a baby’s birth: An estimated 6% of fathers develop paternal depression, but the numbers are triple that among fathers whose children are enrolled in Early Head Start programs, Dr. Bauer said. Paternal depression often co-occurs with postpartum maternal depression, particularly when poverty and substance abuse are contributing factors.

Fewer practitioners may be aware of postpartum anxiety disorders, even though they affect 9%-30% of women. These disorders include generalized anxiety disorder, OCD, and PTSD, either as a preexisting diagnosis or occurring after delivery. Women develop an intensive fear about their child’s well-being and worry that they aren’t able to parent adequately or effectively (Zero to Three. 2009 May:1-6).



Your role in screening mothers

It’s essential that you screen parents for depression, particularly mothers for PPD, because of the potential negative consequences for the child. Research has shown that children of mothers with PPD are at risk for failure to thrive, and have a greater likelihood of mental health conditions, developmental delays, lower IQ scores, sleep problems, and difficulties at school (Infant Behav Dev. 2011 Feb;34[1]:1-14). Further, mothers with PPD are less likely to breastfeed and more likely to stop breastfeeding early, studies have shown (Arch Pediatr Adolesc Med. 2006 Mar;160[3]:279-84).

The risk factors for PPD often occur together, with each additional one adding to the overall risk. As incidence estimates show, teens and those with low income are at higher risk, as are those with less education and any type of additional financial hardship. Other factors that increase women’s risk include interpersonal violence, a lack of social support, a history or family history of anxiety or depression, poor physical or mental health in general, and substance abuse (Depress Anxiety. 2017 Feb;34[2]:178-87).

Dr. Nerissa S. Bauer
Treatment for postpartum depression or anxiety can include medication (typically with SSRIs), therapy, a visit to the patient’s ob.gyn., or referral to crisis intervention or a psychiatrist, psychologist, or other mental health professional.

“Early treatment shows best results,” Dr. Bauer said. Yet less than half of mothers experiencing PPD seek treatment for it.

“Mothers may feel they ‘are strong enough’ and do not need help,” Dr. Bauer said. Or they feel they have to use what limited energy they have on their baby, or they worry about being “labeled as crazy or unable to care for their baby,” she said. Cultural factors also can play a role in this reticence to seek help (Qual Health Res. 2008 Sep;18[9]:1161-73).

“However, mothers are receptive to communication with their child’s pediatrician,” Dr. Bauer said, creating an opportunity for screening that mothers may not otherwise get.
 
 

 

Screening tools and procedures

Despite the risks to infants from maternal depression, less than half of pediatricians screen mothers for PPD, Dr. Bauer said. American Academy of Pediatrics surveys of 778 pediatricians in 2004 and 2013 found that the proportion of pediatricians screening or asking mothers about depression increased from 33% to 44% during that decade, driven partly by the “belief that family screening is in the scope of practice,” she explained. Physicians who asked about the child’s mood were more likely to ask mothers about their mood too, the surveys found (J Dev Behav Pediatr. 2016 Feb-Mar;37[2]:113-20).

Medical organizations differ in their screening recommendations, although all agree screening is important. The American College of Obstetricians and Gynecologists and the U.S. Preventive Services Task Force recommend screening mothers at least once in the perinatal period (Obstet Gynecol. 2015;125:1268–71; JAMA. 2016;315[4]:388-406). The AAP advocates a more aggressive approach, recommending screening at each of the 1, 2, 4, and 6-month child well-visits (“Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents,” 4th Edition [Elk Grove Village, Ill.: American Academy of Pediatrics Publishing, 2017]).

The two preferred screening tools for PPD are the Edinburgh Postpartum Depression Scale (EPDS) and the Patient Health Questionnaire (PHQ).

The former is fast and simple, requiring less than 5 minutes for mothers to answer 10 items about their symptoms in the previous 7 days. The EPDS has a maximum score of 30; anything above 12-13 should prompt further examination or referral. Women scoring a 10 should be reassessed 2 weeks later, unless they answer affirmatively to item 10 on suicidal ideation, in which case they should be referred immediately.

You also can use a shortened form of the EPDS as a first step, asking about the three EPDS items related to anxiety: “self-blame, feeling panicky, and [feeling] anxious or worried for no good reason,” Dr. Bauer said, explaining “the score should be multiplied by 10 and divided by 3, so the cutoff is greater than or equal to 10.”

The PHQ-9 asks about symptoms in the previous 2 weeks. Scores of 10-14 indicate minor depression or mild major depression, and scores of 15-19 indicate moderate depression. Mothers require intervention if they score at least 20, or in the case of teenage mothers, if they score at least 11 or have suicidal thoughts. Like the shortened EPDS-3, the PHQ has a shortened two-question option you can use as surveillance before fully screening mothers: 1. Have you felt down, depressed, or hopeless in the past 2 weeks? 2. Have you felt little interest or pleasure in doing things in the past 2 weeks?

If mothers have a positive screen, Dr. Bauer recommended that practices document it, according to protocols they’ve already set up.

“It’s not unlike domestic violence, maternal substance abuse, or parental smoking habits,” she said. “The score need not be noted, but [should] include details such as the name of the screener used, interpretation of the results, and when a referral was made.”

After making a referral to her ob.gyn. or a mental health professional, you can continue to help mothers by offering support and reassurance, reminding them that they are not alone and not to blame for depression, and that treatment can help them. Encourage parents to seek your advice and support as a pediatrician and use you as a resource to refer them to services that can help, such as lactation consultants and home-visiting programs.

Dr. Bauer offerred the following recommendations for clinical practice:

  • Choose a validated screener for postpartum depression.
  • Share the tool with everyone in your practice.
  • Identify ways to integrate the screening tool into daily work flow.
  • Collect data.
  • Implement and assess how it went after a short time, using plan-do-study-act cycles.

Dr. Bauer advised consulting the following websites for information regarding postpartum depression:

  • AAP Screening and Technical Assistance and Resource (STAR) Center. This AAP website recommends validated screening tools for maternal depression and has them available on the site ().
  • Postpartum Support International (PSI). This website offers information and resources for women, family, and professionals (). PSI can also be reached by calling 800-944-4773.
  • PSI Support Coordinator Network. This network can provide referrals for specialized support, such as for members of the military, for fathers, when there are legal concerns, or when psychosis is present, and serves all 50 states and 40 countries ().
  • PostpartumDads. This website has recommendations for partners of women with postpartum depression, offering recommendations on how dads can help themselves and the mothers ().
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CHICAGO – Screening mothers for postpartum depression is critical, because of the potential negative consequences for the child, according to Nerissa S. Bauer, MD, MPH.

Postpartum depression is the best known mood disorder related to pregnancy, but it’s not the only one. Perinatal mood and anxiety disorders exist along a spectrum, she told attendees at the American Academy of Pediatrics annual meeting. That spectrum includes prenatal depression, prenatal anxiety, “baby blues,” postpartum depression, posttraumatic stress disorder (PSTD), and postpartum anxiety with panic attacks and/or obsessive-compulsive disorder (OCD).

monkeybusinessimages/Thinkstock
Baby blues in mothers after delivery – temporary, mild symptoms of depression that don’t interfere with caring for the baby and aren’t cause for alarm – are a normal occurrence and have been reported worldwide. About 50%-80% of women experience baby blues. These symptoms tend to peak around 5 days post partum. “Pediatricians can provide reassurance, emotional support, and demystification” in helping women cope with baby blues, said Dr. Bauer, a pediatrician at Indiana University, Indianapolis.



Postpartum mood disorders

Postpartum depression (PPD), however, is serious and requires intervention. An estimated 10%-20% of new mothers experience PPD, but the numbers are much higher in at-risk communities. Up to 48% of mothers in low-income households and 40%-60% of adolescent mothers in low-income households experience it. Yet only about 15% of these higher-risk women seek treatment for PPD (Pediatrics. 2010 Nov;126[5]:1032-9).

PPD symptoms are similar to the usual symptoms of a depressive disorder: depressed mood, irritability, changes in sleep and/or appetite, fatigue, sleepiness, loss of interest in activities, inability to feel pleasure in everyday life, guilt, difficulty concentrating, indecisiveness, low energy, despair, and feelings of worthlessness. The biggest difference – and most important symptom – is that women with PPD may have thoughts about harming not only themselves but also their child. This symptom calls for immediate intervention and sometimes can be a sign of postpartum psychosis.

Postpartum psychosis is rare, occurring in about 1-3 out of 1,000 women, but its seriousness requires immediate medical attention, including hospitalization in most cases. The best established risk factor is preexisting bipolar disorder. Postpartum psychosis usually occurs in the first 4 weeks after delivery, with symptoms that include paranoia, severe mood shifts, hallucinations, delusions, and suicidal and/or homicidal thoughts.

Fathers also can experience depression after a baby’s birth: An estimated 6% of fathers develop paternal depression, but the numbers are triple that among fathers whose children are enrolled in Early Head Start programs, Dr. Bauer said. Paternal depression often co-occurs with postpartum maternal depression, particularly when poverty and substance abuse are contributing factors.

Fewer practitioners may be aware of postpartum anxiety disorders, even though they affect 9%-30% of women. These disorders include generalized anxiety disorder, OCD, and PTSD, either as a preexisting diagnosis or occurring after delivery. Women develop an intensive fear about their child’s well-being and worry that they aren’t able to parent adequately or effectively (Zero to Three. 2009 May:1-6).



Your role in screening mothers

It’s essential that you screen parents for depression, particularly mothers for PPD, because of the potential negative consequences for the child. Research has shown that children of mothers with PPD are at risk for failure to thrive, and have a greater likelihood of mental health conditions, developmental delays, lower IQ scores, sleep problems, and difficulties at school (Infant Behav Dev. 2011 Feb;34[1]:1-14). Further, mothers with PPD are less likely to breastfeed and more likely to stop breastfeeding early, studies have shown (Arch Pediatr Adolesc Med. 2006 Mar;160[3]:279-84).

The risk factors for PPD often occur together, with each additional one adding to the overall risk. As incidence estimates show, teens and those with low income are at higher risk, as are those with less education and any type of additional financial hardship. Other factors that increase women’s risk include interpersonal violence, a lack of social support, a history or family history of anxiety or depression, poor physical or mental health in general, and substance abuse (Depress Anxiety. 2017 Feb;34[2]:178-87).

Dr. Nerissa S. Bauer
Treatment for postpartum depression or anxiety can include medication (typically with SSRIs), therapy, a visit to the patient’s ob.gyn., or referral to crisis intervention or a psychiatrist, psychologist, or other mental health professional.

“Early treatment shows best results,” Dr. Bauer said. Yet less than half of mothers experiencing PPD seek treatment for it.

“Mothers may feel they ‘are strong enough’ and do not need help,” Dr. Bauer said. Or they feel they have to use what limited energy they have on their baby, or they worry about being “labeled as crazy or unable to care for their baby,” she said. Cultural factors also can play a role in this reticence to seek help (Qual Health Res. 2008 Sep;18[9]:1161-73).

“However, mothers are receptive to communication with their child’s pediatrician,” Dr. Bauer said, creating an opportunity for screening that mothers may not otherwise get.
 
 

 

Screening tools and procedures

Despite the risks to infants from maternal depression, less than half of pediatricians screen mothers for PPD, Dr. Bauer said. American Academy of Pediatrics surveys of 778 pediatricians in 2004 and 2013 found that the proportion of pediatricians screening or asking mothers about depression increased from 33% to 44% during that decade, driven partly by the “belief that family screening is in the scope of practice,” she explained. Physicians who asked about the child’s mood were more likely to ask mothers about their mood too, the surveys found (J Dev Behav Pediatr. 2016 Feb-Mar;37[2]:113-20).

Medical organizations differ in their screening recommendations, although all agree screening is important. The American College of Obstetricians and Gynecologists and the U.S. Preventive Services Task Force recommend screening mothers at least once in the perinatal period (Obstet Gynecol. 2015;125:1268–71; JAMA. 2016;315[4]:388-406). The AAP advocates a more aggressive approach, recommending screening at each of the 1, 2, 4, and 6-month child well-visits (“Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents,” 4th Edition [Elk Grove Village, Ill.: American Academy of Pediatrics Publishing, 2017]).

The two preferred screening tools for PPD are the Edinburgh Postpartum Depression Scale (EPDS) and the Patient Health Questionnaire (PHQ).

The former is fast and simple, requiring less than 5 minutes for mothers to answer 10 items about their symptoms in the previous 7 days. The EPDS has a maximum score of 30; anything above 12-13 should prompt further examination or referral. Women scoring a 10 should be reassessed 2 weeks later, unless they answer affirmatively to item 10 on suicidal ideation, in which case they should be referred immediately.

You also can use a shortened form of the EPDS as a first step, asking about the three EPDS items related to anxiety: “self-blame, feeling panicky, and [feeling] anxious or worried for no good reason,” Dr. Bauer said, explaining “the score should be multiplied by 10 and divided by 3, so the cutoff is greater than or equal to 10.”

The PHQ-9 asks about symptoms in the previous 2 weeks. Scores of 10-14 indicate minor depression or mild major depression, and scores of 15-19 indicate moderate depression. Mothers require intervention if they score at least 20, or in the case of teenage mothers, if they score at least 11 or have suicidal thoughts. Like the shortened EPDS-3, the PHQ has a shortened two-question option you can use as surveillance before fully screening mothers: 1. Have you felt down, depressed, or hopeless in the past 2 weeks? 2. Have you felt little interest or pleasure in doing things in the past 2 weeks?

If mothers have a positive screen, Dr. Bauer recommended that practices document it, according to protocols they’ve already set up.

“It’s not unlike domestic violence, maternal substance abuse, or parental smoking habits,” she said. “The score need not be noted, but [should] include details such as the name of the screener used, interpretation of the results, and when a referral was made.”

After making a referral to her ob.gyn. or a mental health professional, you can continue to help mothers by offering support and reassurance, reminding them that they are not alone and not to blame for depression, and that treatment can help them. Encourage parents to seek your advice and support as a pediatrician and use you as a resource to refer them to services that can help, such as lactation consultants and home-visiting programs.

Dr. Bauer offerred the following recommendations for clinical practice:

  • Choose a validated screener for postpartum depression.
  • Share the tool with everyone in your practice.
  • Identify ways to integrate the screening tool into daily work flow.
  • Collect data.
  • Implement and assess how it went after a short time, using plan-do-study-act cycles.

Dr. Bauer advised consulting the following websites for information regarding postpartum depression:

  • AAP Screening and Technical Assistance and Resource (STAR) Center. This AAP website recommends validated screening tools for maternal depression and has them available on the site ().
  • Postpartum Support International (PSI). This website offers information and resources for women, family, and professionals (). PSI can also be reached by calling 800-944-4773.
  • PSI Support Coordinator Network. This network can provide referrals for specialized support, such as for members of the military, for fathers, when there are legal concerns, or when psychosis is present, and serves all 50 states and 40 countries ().
  • PostpartumDads. This website has recommendations for partners of women with postpartum depression, offering recommendations on how dads can help themselves and the mothers ().

 

CHICAGO – Screening mothers for postpartum depression is critical, because of the potential negative consequences for the child, according to Nerissa S. Bauer, MD, MPH.

Postpartum depression is the best known mood disorder related to pregnancy, but it’s not the only one. Perinatal mood and anxiety disorders exist along a spectrum, she told attendees at the American Academy of Pediatrics annual meeting. That spectrum includes prenatal depression, prenatal anxiety, “baby blues,” postpartum depression, posttraumatic stress disorder (PSTD), and postpartum anxiety with panic attacks and/or obsessive-compulsive disorder (OCD).

monkeybusinessimages/Thinkstock
Baby blues in mothers after delivery – temporary, mild symptoms of depression that don’t interfere with caring for the baby and aren’t cause for alarm – are a normal occurrence and have been reported worldwide. About 50%-80% of women experience baby blues. These symptoms tend to peak around 5 days post partum. “Pediatricians can provide reassurance, emotional support, and demystification” in helping women cope with baby blues, said Dr. Bauer, a pediatrician at Indiana University, Indianapolis.



Postpartum mood disorders

Postpartum depression (PPD), however, is serious and requires intervention. An estimated 10%-20% of new mothers experience PPD, but the numbers are much higher in at-risk communities. Up to 48% of mothers in low-income households and 40%-60% of adolescent mothers in low-income households experience it. Yet only about 15% of these higher-risk women seek treatment for PPD (Pediatrics. 2010 Nov;126[5]:1032-9).

PPD symptoms are similar to the usual symptoms of a depressive disorder: depressed mood, irritability, changes in sleep and/or appetite, fatigue, sleepiness, loss of interest in activities, inability to feel pleasure in everyday life, guilt, difficulty concentrating, indecisiveness, low energy, despair, and feelings of worthlessness. The biggest difference – and most important symptom – is that women with PPD may have thoughts about harming not only themselves but also their child. This symptom calls for immediate intervention and sometimes can be a sign of postpartum psychosis.

Postpartum psychosis is rare, occurring in about 1-3 out of 1,000 women, but its seriousness requires immediate medical attention, including hospitalization in most cases. The best established risk factor is preexisting bipolar disorder. Postpartum psychosis usually occurs in the first 4 weeks after delivery, with symptoms that include paranoia, severe mood shifts, hallucinations, delusions, and suicidal and/or homicidal thoughts.

Fathers also can experience depression after a baby’s birth: An estimated 6% of fathers develop paternal depression, but the numbers are triple that among fathers whose children are enrolled in Early Head Start programs, Dr. Bauer said. Paternal depression often co-occurs with postpartum maternal depression, particularly when poverty and substance abuse are contributing factors.

Fewer practitioners may be aware of postpartum anxiety disorders, even though they affect 9%-30% of women. These disorders include generalized anxiety disorder, OCD, and PTSD, either as a preexisting diagnosis or occurring after delivery. Women develop an intensive fear about their child’s well-being and worry that they aren’t able to parent adequately or effectively (Zero to Three. 2009 May:1-6).



Your role in screening mothers

It’s essential that you screen parents for depression, particularly mothers for PPD, because of the potential negative consequences for the child. Research has shown that children of mothers with PPD are at risk for failure to thrive, and have a greater likelihood of mental health conditions, developmental delays, lower IQ scores, sleep problems, and difficulties at school (Infant Behav Dev. 2011 Feb;34[1]:1-14). Further, mothers with PPD are less likely to breastfeed and more likely to stop breastfeeding early, studies have shown (Arch Pediatr Adolesc Med. 2006 Mar;160[3]:279-84).

The risk factors for PPD often occur together, with each additional one adding to the overall risk. As incidence estimates show, teens and those with low income are at higher risk, as are those with less education and any type of additional financial hardship. Other factors that increase women’s risk include interpersonal violence, a lack of social support, a history or family history of anxiety or depression, poor physical or mental health in general, and substance abuse (Depress Anxiety. 2017 Feb;34[2]:178-87).

Dr. Nerissa S. Bauer
Treatment for postpartum depression or anxiety can include medication (typically with SSRIs), therapy, a visit to the patient’s ob.gyn., or referral to crisis intervention or a psychiatrist, psychologist, or other mental health professional.

“Early treatment shows best results,” Dr. Bauer said. Yet less than half of mothers experiencing PPD seek treatment for it.

“Mothers may feel they ‘are strong enough’ and do not need help,” Dr. Bauer said. Or they feel they have to use what limited energy they have on their baby, or they worry about being “labeled as crazy or unable to care for their baby,” she said. Cultural factors also can play a role in this reticence to seek help (Qual Health Res. 2008 Sep;18[9]:1161-73).

“However, mothers are receptive to communication with their child’s pediatrician,” Dr. Bauer said, creating an opportunity for screening that mothers may not otherwise get.
 
 

 

Screening tools and procedures

Despite the risks to infants from maternal depression, less than half of pediatricians screen mothers for PPD, Dr. Bauer said. American Academy of Pediatrics surveys of 778 pediatricians in 2004 and 2013 found that the proportion of pediatricians screening or asking mothers about depression increased from 33% to 44% during that decade, driven partly by the “belief that family screening is in the scope of practice,” she explained. Physicians who asked about the child’s mood were more likely to ask mothers about their mood too, the surveys found (J Dev Behav Pediatr. 2016 Feb-Mar;37[2]:113-20).

Medical organizations differ in their screening recommendations, although all agree screening is important. The American College of Obstetricians and Gynecologists and the U.S. Preventive Services Task Force recommend screening mothers at least once in the perinatal period (Obstet Gynecol. 2015;125:1268–71; JAMA. 2016;315[4]:388-406). The AAP advocates a more aggressive approach, recommending screening at each of the 1, 2, 4, and 6-month child well-visits (“Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents,” 4th Edition [Elk Grove Village, Ill.: American Academy of Pediatrics Publishing, 2017]).

The two preferred screening tools for PPD are the Edinburgh Postpartum Depression Scale (EPDS) and the Patient Health Questionnaire (PHQ).

The former is fast and simple, requiring less than 5 minutes for mothers to answer 10 items about their symptoms in the previous 7 days. The EPDS has a maximum score of 30; anything above 12-13 should prompt further examination or referral. Women scoring a 10 should be reassessed 2 weeks later, unless they answer affirmatively to item 10 on suicidal ideation, in which case they should be referred immediately.

You also can use a shortened form of the EPDS as a first step, asking about the three EPDS items related to anxiety: “self-blame, feeling panicky, and [feeling] anxious or worried for no good reason,” Dr. Bauer said, explaining “the score should be multiplied by 10 and divided by 3, so the cutoff is greater than or equal to 10.”

The PHQ-9 asks about symptoms in the previous 2 weeks. Scores of 10-14 indicate minor depression or mild major depression, and scores of 15-19 indicate moderate depression. Mothers require intervention if they score at least 20, or in the case of teenage mothers, if they score at least 11 or have suicidal thoughts. Like the shortened EPDS-3, the PHQ has a shortened two-question option you can use as surveillance before fully screening mothers: 1. Have you felt down, depressed, or hopeless in the past 2 weeks? 2. Have you felt little interest or pleasure in doing things in the past 2 weeks?

If mothers have a positive screen, Dr. Bauer recommended that practices document it, according to protocols they’ve already set up.

“It’s not unlike domestic violence, maternal substance abuse, or parental smoking habits,” she said. “The score need not be noted, but [should] include details such as the name of the screener used, interpretation of the results, and when a referral was made.”

After making a referral to her ob.gyn. or a mental health professional, you can continue to help mothers by offering support and reassurance, reminding them that they are not alone and not to blame for depression, and that treatment can help them. Encourage parents to seek your advice and support as a pediatrician and use you as a resource to refer them to services that can help, such as lactation consultants and home-visiting programs.

Dr. Bauer offerred the following recommendations for clinical practice:

  • Choose a validated screener for postpartum depression.
  • Share the tool with everyone in your practice.
  • Identify ways to integrate the screening tool into daily work flow.
  • Collect data.
  • Implement and assess how it went after a short time, using plan-do-study-act cycles.

Dr. Bauer advised consulting the following websites for information regarding postpartum depression:

  • AAP Screening and Technical Assistance and Resource (STAR) Center. This AAP website recommends validated screening tools for maternal depression and has them available on the site ().
  • Postpartum Support International (PSI). This website offers information and resources for women, family, and professionals (). PSI can also be reached by calling 800-944-4773.
  • PSI Support Coordinator Network. This network can provide referrals for specialized support, such as for members of the military, for fathers, when there are legal concerns, or when psychosis is present, and serves all 50 states and 40 countries ().
  • PostpartumDads. This website has recommendations for partners of women with postpartum depression, offering recommendations on how dads can help themselves and the mothers ().
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ADHD and the role of wellness

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ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.

Case summary

James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.

Discussion

When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.

monkeybusinessimages/Thinkstock
In our clinic, we talk with every family not only about treating the emotional and behavioral challenges a family faces, but also about the importance of promoting positive aspects of life that are known to affect the brain. Our domains of wellness include exercise, mindfulness, reading, music, healthy sleep, healthy eating, positive parenting, and community involvement. I would like to focus on three of these – exercise, healthy sleep, and positive parenting – for which there is at least preliminary evidence of beneficial effects on either the core symptoms of ADHD or a common comorbidity, oppositional behavior.
 

Exercise

Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.

Sleep

Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.

Parent training

Dr. Allison Y. Hall
Finally, behavioral parent training repeatedly has been demonstrated to be effective for the oppositional behavior so common with ADHD. Specific skills also can be used to help motivate children with things like homework. I emphasize that children with ADHD are quite challenging to parents, and we all can use extra skills to support them. CHADD, the national ADHD organization, offers a program called Parent to Parent that offers peer support, education about ADHD, and training in the specific behavioral skills. This is offered locally in many areas, and also can be accessed online at www.chadd.org by searching for Parent to Parent.

Treatment plan

1. Have the child exercise 1 hour every day. Have fun!

2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.

3. Check out the CHADD website for Parent to Parent.

4. Start a trial of stimulant medication.

5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.

 

 

When to refer

Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.

Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.

References

1. Child Care Health Dev. 2015 Nov;41(6):779-88.

2. BMJ. 2015. doi: 10.1136/bmj.h68.

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ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.

Case summary

James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.

Discussion

When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.

monkeybusinessimages/Thinkstock
In our clinic, we talk with every family not only about treating the emotional and behavioral challenges a family faces, but also about the importance of promoting positive aspects of life that are known to affect the brain. Our domains of wellness include exercise, mindfulness, reading, music, healthy sleep, healthy eating, positive parenting, and community involvement. I would like to focus on three of these – exercise, healthy sleep, and positive parenting – for which there is at least preliminary evidence of beneficial effects on either the core symptoms of ADHD or a common comorbidity, oppositional behavior.
 

Exercise

Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.

Sleep

Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.

Parent training

Dr. Allison Y. Hall
Finally, behavioral parent training repeatedly has been demonstrated to be effective for the oppositional behavior so common with ADHD. Specific skills also can be used to help motivate children with things like homework. I emphasize that children with ADHD are quite challenging to parents, and we all can use extra skills to support them. CHADD, the national ADHD organization, offers a program called Parent to Parent that offers peer support, education about ADHD, and training in the specific behavioral skills. This is offered locally in many areas, and also can be accessed online at www.chadd.org by searching for Parent to Parent.

Treatment plan

1. Have the child exercise 1 hour every day. Have fun!

2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.

3. Check out the CHADD website for Parent to Parent.

4. Start a trial of stimulant medication.

5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.

 

 

When to refer

Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.

Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.

References

1. Child Care Health Dev. 2015 Nov;41(6):779-88.

2. BMJ. 2015. doi: 10.1136/bmj.h68.

 

ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.

Case summary

James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.

Discussion

When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.

monkeybusinessimages/Thinkstock
In our clinic, we talk with every family not only about treating the emotional and behavioral challenges a family faces, but also about the importance of promoting positive aspects of life that are known to affect the brain. Our domains of wellness include exercise, mindfulness, reading, music, healthy sleep, healthy eating, positive parenting, and community involvement. I would like to focus on three of these – exercise, healthy sleep, and positive parenting – for which there is at least preliminary evidence of beneficial effects on either the core symptoms of ADHD or a common comorbidity, oppositional behavior.
 

Exercise

Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.

Sleep

Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.

Parent training

Dr. Allison Y. Hall
Finally, behavioral parent training repeatedly has been demonstrated to be effective for the oppositional behavior so common with ADHD. Specific skills also can be used to help motivate children with things like homework. I emphasize that children with ADHD are quite challenging to parents, and we all can use extra skills to support them. CHADD, the national ADHD organization, offers a program called Parent to Parent that offers peer support, education about ADHD, and training in the specific behavioral skills. This is offered locally in many areas, and also can be accessed online at www.chadd.org by searching for Parent to Parent.

Treatment plan

1. Have the child exercise 1 hour every day. Have fun!

2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.

3. Check out the CHADD website for Parent to Parent.

4. Start a trial of stimulant medication.

5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.

 

 

When to refer

Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.

Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.

References

1. Child Care Health Dev. 2015 Nov;41(6):779-88.

2. BMJ. 2015. doi: 10.1136/bmj.h68.

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