Opinion

 

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at pdnews@mdedge.com.

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

 

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at pdnews@mdedge.com.

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

 

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at pdnews@mdedge.com.

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

In a recent article on this website, Jake Remaly reports on a study suggesting that maternal migraine is associated with infant colic. In a presentation at the annual meeting of the American Headache Society, Amy Gelfand, MD, a neurologist at the University of California, San Francisco, reported the results of a national survey of more than 1,400 parents (827 mothers, 592 fathers) collected via social media. She and her colleagues found that mothers with migraine were more likely to have an infant with colic, with an odds ratio of 1.7 that increased to 2.5 for mothers with more frequent migraine. Fathers with migraine were no more likely to have an infant with colic.

AntonioGuillem/Gety Images

In a video clip included in the article, Dr. Gelfand discusses the possibilities that she and her group considered as they attempted to explain the study’s findings. Are there such things as “migraine genes?” If so, the failure to discover a paternal association might suggest that these would be mitochondrial genes. The researchers wondered if a substance in breast milk was acting as trigger, but they found that the association between colic and migraine was unrelated to whether the baby was fed by breast or bottle.

In full disclosure, I was not one of the investigators. Neither my wife nor I have migraine, and although our children cried as infants, they wouldn’t have qualified as having colic. However, I spent more than 40 years immersed in more than 300,000 patient encounters and can claim membership in the International Brother/Sisterhood of Anecdotal Observers. And, as such will offer up my explanation for Dr. Gelfand’s findings.

It is clear to me that most, if not all, children with migraine have their headaches when they are sleep deprived. While my sample size is smaller, I believe the same association also is true for many of the adults I know who have migraine. At least in children, restorative sleep ends the migraine much as it does for an epileptic seizure.

Traditionally, colic has been thought to be somehow related to a gastrointestinal phenomenon by many extended family members and some physicians. However, in my experience, it is usually a symptom of sleep deprivation compounded by the failure of those around the children to realize the obvious and take appropriate action. Of course, some babies are reacting to sore tummies, but my guess is that most are having headaches. We may never know. Dr. Gelfand also shares my observation that colicky crying is more likely to occur “at the end of the day,” a time when we are tired and are less tolerant of overstimulation.

For decades, I have been convinced that migraine and colic are the same pathophysiologic process. However, the presentation varies depending on the age of the patients. Remember, infants can’t talk. It already has been shown that adults with migraine often were more likely to have been colicky infants. (Dr. Gelfand mentions this as well.) These unfortunate individuals probably have inherited a vulnerability to sleep deprivation that manifests itself as a headache. I hope to live long enough to be around when someone discovers the wrinkle in the genome that creates this vulnerability.

So, why did the researchers fail to find an association between fathers and colic? The answer is simple. We fathers are beginning to take on a larger role in parenting of infants and like to complain about how difficult it is. However, it is mothers who still have the lioness’ share of the work. They lose the most sleep and are starting off parenthood with 9 months of less than optimal sleep followed by who knows how many hours of energy-sapping labor. It’s surprising they all don’t have migraines.
 

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

In a recent article on this website, Jake Remaly reports on a study suggesting that maternal migraine is associated with infant colic. In a presentation at the annual meeting of the American Headache Society, Amy Gelfand, MD, a neurologist at the University of California, San Francisco, reported the results of a national survey of more than 1,400 parents (827 mothers, 592 fathers) collected via social media. She and her colleagues found that mothers with migraine were more likely to have an infant with colic, with an odds ratio of 1.7 that increased to 2.5 for mothers with more frequent migraine. Fathers with migraine were no more likely to have an infant with colic.

AntonioGuillem/Gety Images

In a video clip included in the article, Dr. Gelfand discusses the possibilities that she and her group considered as they attempted to explain the study’s findings. Are there such things as “migraine genes?” If so, the failure to discover a paternal association might suggest that these would be mitochondrial genes. The researchers wondered if a substance in breast milk was acting as trigger, but they found that the association between colic and migraine was unrelated to whether the baby was fed by breast or bottle.

In full disclosure, I was not one of the investigators. Neither my wife nor I have migraine, and although our children cried as infants, they wouldn’t have qualified as having colic. However, I spent more than 40 years immersed in more than 300,000 patient encounters and can claim membership in the International Brother/Sisterhood of Anecdotal Observers. And, as such will offer up my explanation for Dr. Gelfand’s findings.

It is clear to me that most, if not all, children with migraine have their headaches when they are sleep deprived. While my sample size is smaller, I believe the same association also is true for many of the adults I know who have migraine. At least in children, restorative sleep ends the migraine much as it does for an epileptic seizure.

Traditionally, colic has been thought to be somehow related to a gastrointestinal phenomenon by many extended family members and some physicians. However, in my experience, it is usually a symptom of sleep deprivation compounded by the failure of those around the children to realize the obvious and take appropriate action. Of course, some babies are reacting to sore tummies, but my guess is that most are having headaches. We may never know. Dr. Gelfand also shares my observation that colicky crying is more likely to occur “at the end of the day,” a time when we are tired and are less tolerant of overstimulation.

For decades, I have been convinced that migraine and colic are the same pathophysiologic process. However, the presentation varies depending on the age of the patients. Remember, infants can’t talk. It already has been shown that adults with migraine often were more likely to have been colicky infants. (Dr. Gelfand mentions this as well.) These unfortunate individuals probably have inherited a vulnerability to sleep deprivation that manifests itself as a headache. I hope to live long enough to be around when someone discovers the wrinkle in the genome that creates this vulnerability.

So, why did the researchers fail to find an association between fathers and colic? The answer is simple. We fathers are beginning to take on a larger role in parenting of infants and like to complain about how difficult it is. However, it is mothers who still have the lioness’ share of the work. They lose the most sleep and are starting off parenthood with 9 months of less than optimal sleep followed by who knows how many hours of energy-sapping labor. It’s surprising they all don’t have migraines.
 

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

In a recent article on this website, Jake Remaly reports on a study suggesting that maternal migraine is associated with infant colic. In a presentation at the annual meeting of the American Headache Society, Amy Gelfand, MD, a neurologist at the University of California, San Francisco, reported the results of a national survey of more than 1,400 parents (827 mothers, 592 fathers) collected via social media. She and her colleagues found that mothers with migraine were more likely to have an infant with colic, with an odds ratio of 1.7 that increased to 2.5 for mothers with more frequent migraine. Fathers with migraine were no more likely to have an infant with colic.

AntonioGuillem/Gety Images

In a video clip included in the article, Dr. Gelfand discusses the possibilities that she and her group considered as they attempted to explain the study’s findings. Are there such things as “migraine genes?” If so, the failure to discover a paternal association might suggest that these would be mitochondrial genes. The researchers wondered if a substance in breast milk was acting as trigger, but they found that the association between colic and migraine was unrelated to whether the baby was fed by breast or bottle.

In full disclosure, I was not one of the investigators. Neither my wife nor I have migraine, and although our children cried as infants, they wouldn’t have qualified as having colic. However, I spent more than 40 years immersed in more than 300,000 patient encounters and can claim membership in the International Brother/Sisterhood of Anecdotal Observers. And, as such will offer up my explanation for Dr. Gelfand’s findings.

It is clear to me that most, if not all, children with migraine have their headaches when they are sleep deprived. While my sample size is smaller, I believe the same association also is true for many of the adults I know who have migraine. At least in children, restorative sleep ends the migraine much as it does for an epileptic seizure.

Traditionally, colic has been thought to be somehow related to a gastrointestinal phenomenon by many extended family members and some physicians. However, in my experience, it is usually a symptom of sleep deprivation compounded by the failure of those around the children to realize the obvious and take appropriate action. Of course, some babies are reacting to sore tummies, but my guess is that most are having headaches. We may never know. Dr. Gelfand also shares my observation that colicky crying is more likely to occur “at the end of the day,” a time when we are tired and are less tolerant of overstimulation.

For decades, I have been convinced that migraine and colic are the same pathophysiologic process. However, the presentation varies depending on the age of the patients. Remember, infants can’t talk. It already has been shown that adults with migraine often were more likely to have been colicky infants. (Dr. Gelfand mentions this as well.) These unfortunate individuals probably have inherited a vulnerability to sleep deprivation that manifests itself as a headache. I hope to live long enough to be around when someone discovers the wrinkle in the genome that creates this vulnerability.

So, why did the researchers fail to find an association between fathers and colic? The answer is simple. We fathers are beginning to take on a larger role in parenting of infants and like to complain about how difficult it is. However, it is mothers who still have the lioness’ share of the work. They lose the most sleep and are starting off parenthood with 9 months of less than optimal sleep followed by who knows how many hours of energy-sapping labor. It’s surprising they all don’t have migraines.
 

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

 

Carla is an otherwise-healthy 14-year-old female followed by her pediatrician for symptoms of depression and anxiety that have worsened over the past 8 months. Anhedonia, irritability, poor concentration, fatigue, hypersomnolence, and significant weight gain have increasingly led to further dysphoria, social isolation, and obsessive rumination, all of which now contribute to more dysfunction in both her home and school life. Based on Carla’s apprehension over “taking pills,” she was referred for outpatient therapy 5 months ago but because of difficulty maintaining weekly appointments, she stopped attending after 6 weeks, citing difficulty aligning with her therapist.

Carla was seen in an urgent, unscheduled follow-up appointment 2 months prior to address increased thoughts of wishing to be dead. She had neither a plan nor a desire to act on these ideations. During an interview, she was distant with poor eye contact, and her affect was notably blunted. Her mother, who had accompanied her in the waiting room, expressed frustration to the nurse about discovering that Carla was using cannabis, that she often appeared aloof and unmotivated to do much of anything but “sit in her room and play on her phone for hours on end.” She compared Carla with her ex-husband, who had similar mood swings that often led to erratic and violent outbursts towards Carla and her mother, behaviors that ultimately led them to leave him when Carla was 6 years old.

After a discussion over the risks and benefits of various treatment options, Carla was started on low-dose fluoxetine with a plan to titrate the medication after 2 weeks. A referral for outpatient substance use treatment also was initiated. Carla’s mother telephoned 10 days later in an update that things have drastically improved in Carla’s mood and activity. The following week her mother called back again with concerns that Carla is no longer sleeping, appears restless, impulsive, and disinhibited.

Discussion

Carla’s initial presentation is common to primary care settings. Based on her earliest reported symptoms, she would qualify for a diagnosis of major depression. Decisions regarding initial treatment for children and adolescents must take into account the severity of symptoms, risks, autonomy of the patient and family, as well as available evidence. Her response to outpatient therapy is not an anomaly. With an ever-increasing demand on mental health services, the availability of consistent, quality outpatient therapy for this population is not always easy to secure.^1,2 Combining targeted therapy with pharmacologic interventions for major depression appear to have the most effective outcomes.³

Carla’s progression also illustrates the challenges and potential pitfalls of attempting to understand and address her symptoms according to a single nosology. Depression is a like a fever. It can be caused by a myriad of factors and, left to linger, may lead to further residual complications. Focusing attention to her symptoms also may lead to a differential including adjustment problems, social anxiety, effects of trauma, surreptitious substance use, or even bipolar depression. Understanding Carla’s (or anyone else’s) unique predispositions to illness will better optimize the course of treatment.

To begin with, a clear delineation of Carla’s historic symptoms and any possible medical contributions to her presentation are necessary to investigate. Specific inquiries into past episodes of activation including hyperarousal, impulsivity, restlessness, and insomnia should be elucidated prior to consideration of medication selection.⁴ Considering Carla’s age and the known association between antidepressant-induced manic conversion among children aged 10-14 years,⁵ any pharmacologic intervention will benefit from the maxim “start low and go slow.” Her symptoms of activation arise within the setting of titration of an antidepressant. This may raise considerations to her specific metabolism and physiological concentrations of the medication as well as cumulative day exposure.

Complementary to Carla’s own history is that of family members. Often obtaining a reliable family psychiatric history is an exercise fraught with bias, vagueness, and generalizations.⁶ However, given the known heritability of bipolar disorders and the implications for treating depression in such individuals, compared with unipolar depressive symptoms, clarifying the nature of family illness may elucidate potential susceptibilities previously unconsidered.⁷ In this case, descriptions of Carla’s father’s behavior raise concerns for underlying bipolar disorder, as do the accounts of traumatic stress exposure and their compounded preponderance for increased suicide risk.⁸

Unfortunately, Carla’s current environmental cues and maladaptive behaviors may be perpetuating her symptoms and possibly placing her on a trajectory for further illness. Exploration of her relationship with her caregivers regarding the interpretation of her symptoms, and need for treatment should be undertaken so as to expand supportive roles. Education regarding cannabis use among adolescents and age-specific risks for later depression, anxiety, and suicide is warranted in a climate when accessibility is on the rise.⁹ Whether or not cannabis use itself leads to amotivation is the subject of current debate.¹⁰ A growing body of evidence is clearly illustrating that Carla’s sedentary behaviors and perceived loneliness likely exacerbate her mental well-being. Such patterns indicate the need for environmental intervention to change such cycles.

Finally, Carla’s progression through treatment speak to the need for open and honest discussions regarding realistic benefits as well potential risks. Progressive symptoms of depression left untreated can be life-threatening themselves, just as effects of activation as described in the vignette above can easily and quickly progress into situations that pose safety concerns. Amidst such periods of intervention, close communication and follow up with patients and their supports ameliorate potential adverse events and lead to better outcomes.

Outcome

Carla’s mother was advised to discontinue the medication, closely monitor Carla’s behavior and sleep, and schedule an emergent follow-up appointment for the next day. A safety plan indicating circumstances in which Carla would require closer medical supervision for safety was reviewed with her mother. Carla was later initiated on lamotrigine and restarted interpersonal therapy.

References

1. N Engl J Med. 2015 May 21;372(21):2029-38.

2. J Pediatr. 2010 Nov;157(5):848-51.

3. Arch Gen Psychiatry. 2007 Oct;64(10):1132-43.

4. Curr Probl Pediatr Adolesc Health Care. 2018 Feb;48(2):50-62.

5. Arch Pediatr Adolesc Med. 2004 Aug;158(8):773-80.

6. Can J Psychiatry. 1993 Nov;38(9):590-4.

7. Appl Clin Genet. 2014 Feb 12;7:33-42.

8. J Am Acad Child Adolesc Psychiatry. 2017 Dec;56(12):1073-1080.

9. JAMA Psychiatry. 2019;76(4):426-34.

10. Subst Use Misuse. 2018 Jun 7;53(7):1158-69.

 

Carla is an otherwise-healthy 14-year-old female followed by her pediatrician for symptoms of depression and anxiety that have worsened over the past 8 months. Anhedonia, irritability, poor concentration, fatigue, hypersomnolence, and significant weight gain have increasingly led to further dysphoria, social isolation, and obsessive rumination, all of which now contribute to more dysfunction in both her home and school life. Based on Carla’s apprehension over “taking pills,” she was referred for outpatient therapy 5 months ago but because of difficulty maintaining weekly appointments, she stopped attending after 6 weeks, citing difficulty aligning with her therapist.

Carla was seen in an urgent, unscheduled follow-up appointment 2 months prior to address increased thoughts of wishing to be dead. She had neither a plan nor a desire to act on these ideations. During an interview, she was distant with poor eye contact, and her affect was notably blunted. Her mother, who had accompanied her in the waiting room, expressed frustration to the nurse about discovering that Carla was using cannabis, that she often appeared aloof and unmotivated to do much of anything but “sit in her room and play on her phone for hours on end.” She compared Carla with her ex-husband, who had similar mood swings that often led to erratic and violent outbursts towards Carla and her mother, behaviors that ultimately led them to leave him when Carla was 6 years old.

After a discussion over the risks and benefits of various treatment options, Carla was started on low-dose fluoxetine with a plan to titrate the medication after 2 weeks. A referral for outpatient substance use treatment also was initiated. Carla’s mother telephoned 10 days later in an update that things have drastically improved in Carla’s mood and activity. The following week her mother called back again with concerns that Carla is no longer sleeping, appears restless, impulsive, and disinhibited.

Discussion

Carla’s initial presentation is common to primary care settings. Based on her earliest reported symptoms, she would qualify for a diagnosis of major depression. Decisions regarding initial treatment for children and adolescents must take into account the severity of symptoms, risks, autonomy of the patient and family, as well as available evidence. Her response to outpatient therapy is not an anomaly. With an ever-increasing demand on mental health services, the availability of consistent, quality outpatient therapy for this population is not always easy to secure.^1,2 Combining targeted therapy with pharmacologic interventions for major depression appear to have the most effective outcomes.³

Carla’s progression also illustrates the challenges and potential pitfalls of attempting to understand and address her symptoms according to a single nosology. Depression is a like a fever. It can be caused by a myriad of factors and, left to linger, may lead to further residual complications. Focusing attention to her symptoms also may lead to a differential including adjustment problems, social anxiety, effects of trauma, surreptitious substance use, or even bipolar depression. Understanding Carla’s (or anyone else’s) unique predispositions to illness will better optimize the course of treatment.

To begin with, a clear delineation of Carla’s historic symptoms and any possible medical contributions to her presentation are necessary to investigate. Specific inquiries into past episodes of activation including hyperarousal, impulsivity, restlessness, and insomnia should be elucidated prior to consideration of medication selection.⁴ Considering Carla’s age and the known association between antidepressant-induced manic conversion among children aged 10-14 years,⁵ any pharmacologic intervention will benefit from the maxim “start low and go slow.” Her symptoms of activation arise within the setting of titration of an antidepressant. This may raise considerations to her specific metabolism and physiological concentrations of the medication as well as cumulative day exposure.

Complementary to Carla’s own history is that of family members. Often obtaining a reliable family psychiatric history is an exercise fraught with bias, vagueness, and generalizations.⁶ However, given the known heritability of bipolar disorders and the implications for treating depression in such individuals, compared with unipolar depressive symptoms, clarifying the nature of family illness may elucidate potential susceptibilities previously unconsidered.⁷ In this case, descriptions of Carla’s father’s behavior raise concerns for underlying bipolar disorder, as do the accounts of traumatic stress exposure and their compounded preponderance for increased suicide risk.⁸

Unfortunately, Carla’s current environmental cues and maladaptive behaviors may be perpetuating her symptoms and possibly placing her on a trajectory for further illness. Exploration of her relationship with her caregivers regarding the interpretation of her symptoms, and need for treatment should be undertaken so as to expand supportive roles. Education regarding cannabis use among adolescents and age-specific risks for later depression, anxiety, and suicide is warranted in a climate when accessibility is on the rise.⁹ Whether or not cannabis use itself leads to amotivation is the subject of current debate.¹⁰ A growing body of evidence is clearly illustrating that Carla’s sedentary behaviors and perceived loneliness likely exacerbate her mental well-being. Such patterns indicate the need for environmental intervention to change such cycles.

Finally, Carla’s progression through treatment speak to the need for open and honest discussions regarding realistic benefits as well potential risks. Progressive symptoms of depression left untreated can be life-threatening themselves, just as effects of activation as described in the vignette above can easily and quickly progress into situations that pose safety concerns. Amidst such periods of intervention, close communication and follow up with patients and their supports ameliorate potential adverse events and lead to better outcomes.

Outcome

Carla’s mother was advised to discontinue the medication, closely monitor Carla’s behavior and sleep, and schedule an emergent follow-up appointment for the next day. A safety plan indicating circumstances in which Carla would require closer medical supervision for safety was reviewed with her mother. Carla was later initiated on lamotrigine and restarted interpersonal therapy.

References

1. N Engl J Med. 2015 May 21;372(21):2029-38.

2. J Pediatr. 2010 Nov;157(5):848-51.

3. Arch Gen Psychiatry. 2007 Oct;64(10):1132-43.

4. Curr Probl Pediatr Adolesc Health Care. 2018 Feb;48(2):50-62.

5. Arch Pediatr Adolesc Med. 2004 Aug;158(8):773-80.

6. Can J Psychiatry. 1993 Nov;38(9):590-4.

7. Appl Clin Genet. 2014 Feb 12;7:33-42.

8. J Am Acad Child Adolesc Psychiatry. 2017 Dec;56(12):1073-1080.

9. JAMA Psychiatry. 2019;76(4):426-34.

10. Subst Use Misuse. 2018 Jun 7;53(7):1158-69.

 

Carla is an otherwise-healthy 14-year-old female followed by her pediatrician for symptoms of depression and anxiety that have worsened over the past 8 months. Anhedonia, irritability, poor concentration, fatigue, hypersomnolence, and significant weight gain have increasingly led to further dysphoria, social isolation, and obsessive rumination, all of which now contribute to more dysfunction in both her home and school life. Based on Carla’s apprehension over “taking pills,” she was referred for outpatient therapy 5 months ago but because of difficulty maintaining weekly appointments, she stopped attending after 6 weeks, citing difficulty aligning with her therapist.

Carla was seen in an urgent, unscheduled follow-up appointment 2 months prior to address increased thoughts of wishing to be dead. She had neither a plan nor a desire to act on these ideations. During an interview, she was distant with poor eye contact, and her affect was notably blunted. Her mother, who had accompanied her in the waiting room, expressed frustration to the nurse about discovering that Carla was using cannabis, that she often appeared aloof and unmotivated to do much of anything but “sit in her room and play on her phone for hours on end.” She compared Carla with her ex-husband, who had similar mood swings that often led to erratic and violent outbursts towards Carla and her mother, behaviors that ultimately led them to leave him when Carla was 6 years old.

After a discussion over the risks and benefits of various treatment options, Carla was started on low-dose fluoxetine with a plan to titrate the medication after 2 weeks. A referral for outpatient substance use treatment also was initiated. Carla’s mother telephoned 10 days later in an update that things have drastically improved in Carla’s mood and activity. The following week her mother called back again with concerns that Carla is no longer sleeping, appears restless, impulsive, and disinhibited.

Discussion

Carla’s initial presentation is common to primary care settings. Based on her earliest reported symptoms, she would qualify for a diagnosis of major depression. Decisions regarding initial treatment for children and adolescents must take into account the severity of symptoms, risks, autonomy of the patient and family, as well as available evidence. Her response to outpatient therapy is not an anomaly. With an ever-increasing demand on mental health services, the availability of consistent, quality outpatient therapy for this population is not always easy to secure.^1,2 Combining targeted therapy with pharmacologic interventions for major depression appear to have the most effective outcomes.³

Carla’s progression also illustrates the challenges and potential pitfalls of attempting to understand and address her symptoms according to a single nosology. Depression is a like a fever. It can be caused by a myriad of factors and, left to linger, may lead to further residual complications. Focusing attention to her symptoms also may lead to a differential including adjustment problems, social anxiety, effects of trauma, surreptitious substance use, or even bipolar depression. Understanding Carla’s (or anyone else’s) unique predispositions to illness will better optimize the course of treatment.

To begin with, a clear delineation of Carla’s historic symptoms and any possible medical contributions to her presentation are necessary to investigate. Specific inquiries into past episodes of activation including hyperarousal, impulsivity, restlessness, and insomnia should be elucidated prior to consideration of medication selection.⁴ Considering Carla’s age and the known association between antidepressant-induced manic conversion among children aged 10-14 years,⁵ any pharmacologic intervention will benefit from the maxim “start low and go slow.” Her symptoms of activation arise within the setting of titration of an antidepressant. This may raise considerations to her specific metabolism and physiological concentrations of the medication as well as cumulative day exposure.

Complementary to Carla’s own history is that of family members. Often obtaining a reliable family psychiatric history is an exercise fraught with bias, vagueness, and generalizations.⁶ However, given the known heritability of bipolar disorders and the implications for treating depression in such individuals, compared with unipolar depressive symptoms, clarifying the nature of family illness may elucidate potential susceptibilities previously unconsidered.⁷ In this case, descriptions of Carla’s father’s behavior raise concerns for underlying bipolar disorder, as do the accounts of traumatic stress exposure and their compounded preponderance for increased suicide risk.⁸

Unfortunately, Carla’s current environmental cues and maladaptive behaviors may be perpetuating her symptoms and possibly placing her on a trajectory for further illness. Exploration of her relationship with her caregivers regarding the interpretation of her symptoms, and need for treatment should be undertaken so as to expand supportive roles. Education regarding cannabis use among adolescents and age-specific risks for later depression, anxiety, and suicide is warranted in a climate when accessibility is on the rise.⁹ Whether or not cannabis use itself leads to amotivation is the subject of current debate.¹⁰ A growing body of evidence is clearly illustrating that Carla’s sedentary behaviors and perceived loneliness likely exacerbate her mental well-being. Such patterns indicate the need for environmental intervention to change such cycles.

Finally, Carla’s progression through treatment speak to the need for open and honest discussions regarding realistic benefits as well potential risks. Progressive symptoms of depression left untreated can be life-threatening themselves, just as effects of activation as described in the vignette above can easily and quickly progress into situations that pose safety concerns. Amidst such periods of intervention, close communication and follow up with patients and their supports ameliorate potential adverse events and lead to better outcomes.

Outcome

Carla’s mother was advised to discontinue the medication, closely monitor Carla’s behavior and sleep, and schedule an emergent follow-up appointment for the next day. A safety plan indicating circumstances in which Carla would require closer medical supervision for safety was reviewed with her mother. Carla was later initiated on lamotrigine and restarted interpersonal therapy.

References

1. N Engl J Med. 2015 May 21;372(21):2029-38.

2. J Pediatr. 2010 Nov;157(5):848-51.

3. Arch Gen Psychiatry. 2007 Oct;64(10):1132-43.

4. Curr Probl Pediatr Adolesc Health Care. 2018 Feb;48(2):50-62.

5. Arch Pediatr Adolesc Med. 2004 Aug;158(8):773-80.

6. Can J Psychiatry. 1993 Nov;38(9):590-4.

7. Appl Clin Genet. 2014 Feb 12;7:33-42.

8. J Am Acad Child Adolesc Psychiatry. 2017 Dec;56(12):1073-1080.

9. JAMA Psychiatry. 2019;76(4):426-34.

10. Subst Use Misuse. 2018 Jun 7;53(7):1158-69.

 

Question: A patient died unexpectedly during hospitalization for a diabetic foot infection. The autopsy revealed the presence of a large saddle pulmonary embolus. The hospital’s peer review committee met to determine if care was suboptimal and whether prophylactic anticoagulation should have been used. When the attending doctor was subsequently sued for malpractice, the plaintiff’s attorney sought to subpoena all of the medical records, including the minutes of the peer review committee. Given this hypothetical scenario, which of the following can occur?

A. “Discovery” is the legal term given to the process during the pretrial phase for amassing relevant documents and other information.

B. A subpoena duces tecum, which is a court order for the production of relevant documents and one that should normally be obeyed, may be issued.

C. The hospital declines to hand over certain types of hospital records, such as peer review minutes, which in this case are statutorily protected from discovery.

D. The plaintiff attorney goes to the judge for an order to compel production and may or may not be successful.

E. All are correct.
 

Answer: E. Physicians and other participants regularly meet, under strict confidential conditions, to discuss adverse events that occur in their institution. Congress and state legislatures have enacted laws to ensure the confidentiality of medical peer review, incident reports, and patient safety work products. Such records are protected from “discovery,” which is a pretrial procedure for collecting evidence in preparation for trial. The rationale for keeping these records beyond the reach of the discovery process is to encourage participants to engage in candid and free-rein analysis of adverse medical events so as to avoid future mishaps. If the content and nature of these discussions were freely available to parties in litigation, there would be a natural reluctance to express one’s viewpoints in a forthright manner.

Any given state’s statute on discovery requires careful reading because it could differ from another state’s directive – with important legal consequences. As an example, Hawaii’s statute¹ contains several inclusions and exclusions and reads in part: “... the information and data protected shall include proceedings and records of a peer review committee, hospital quality assurance committee, or health care review organization that include recordings, transcripts, minutes, and summaries of meetings, conversations, notes, materials, or reports created for, by, or at the direction of a peer review committee, quality assurance committee, or a health care review organization when related to a medical error reporting system. ... Information and data protected from discovery shall not include incident reports, occurrence reports, statements, or similar reports that state facts concerning a specific situation and shall not include records made in the regular course of business by a hospital ... including patient medical records. Original sources of information ... shall not be construed as being immune from discovery ... merely because they were reviewed ... or were in fact submitted to, a health care review organization.”

Predictably, plaintiff attorneys in a medical malpractice lawsuit will attempt to discover information regarding adverse events, hoping to learn about potential errors and judgment lapses, and thus gain an advantage over the defendant doctor and/or hospital. Several recent court cases highlight the contentious nature regarding whether a particular hospital report is to be deemed discoverable. Organized medicine, led by the American Medical Association, has mounted a vigorous response in arguing against the release of peer review and patient safety documents.

The AMA² recently weighed in on the case of Daley v. Teruel and Ingalls Memorial Hospital. In 2013, a renal failure patient died in an Illinois hospital from injuries that arose from prolonged hypoglycemia. She had received insulin, but when her blood glucose dropped to 16 mg/dl, the treatment team was not alerted and she was later found unresponsive with irreversible brain damage. The issue was whether incident reports from the case that were submitted to a certified PSO (patient safety organization) could be discovered. The Federal Patient Safety and Quality Improvement Act (PSQIA) had created PSOs to aggregate data from multiple sources to reduce adverse events and errors and improve medication safety.

An Illinois lower court ruled that, as part of the discovery process, the hospital had to turn over the report. However, the Illinois Appellate Court ruled in favor of the hospital, holding that the PSQIA protects the report because it is a “patient safety work product.”³ The AMA amicus brief had emphasized that Congress created a safeguarded patient safety process under the PSQIA to encourage hospitals to submit patient safety outcomes without fear of increased liability risk and that “these voluntarily created materials should be used for their intended purpose, not as a roadmap for litigation.”

New Jersey has also ruled against the discovery of a hospital’s self-critical report of a patient’s care, prepared in accordance with New Jersey’s Patient Safety Act.⁴ The plaintiff alleged that, when she reported to the emergency room at Chilton Medical Center complaining of persistent abdominal pain, fever, body aches, weakness, and a phlegmatic cough, she was incorrectly diagnosed as having pneumonia. In fact, she had appendicitis and a pelvic abscess. The New Jersey Supreme Court affirmed the panel’s order shielding the redacted document from discovery, but it reversed the judgment to the extent it ended the defendants’ discovery obligation with respect to this dispute, requiring instead that the lower court address, through current discovery rules, the proper balancing of interests between requesting and responding parties.

In a recent Michigan case,⁵ the trial court had earlier ruled that peer review documents at issue were in fact discoverable. Like similar statutes elsewhere, Michigan’s peer review privileges serve to encourage participation to improve on patient morbidity and mortality. The case centered on a court order compelling a Michigan hospital to release a physician’s credentialing file in a medical liability lawsuit on the narrow basis that the nondiscoverability privilege applied only to peer review deliberations and was inapplicable in the case. The trial judge had opined that, if all materials viewed by peer review committees were deemed undiscoverable, a hospital could never be held accountable for any negligent act within the purview of the committee. In its amicus brief in support of the hospital, the AMA argued that Michigan’s peer review privilege has historically spanned the bounds of the actual peer review process, and it countered that hospitals can be held liable – and are regularly held liable – without opening up these documents and that plaintiffs can use the same discovery mechanisms generally available to plaintiffs in other lawsuits.⁶ The case is currently under appeal.

In contrast, at least two state supreme courts have ruled to limit protections from discovery. The Florida Supreme Court has held that the federal law was intended to improve overall health care rather than to act as a shield to providers. In a case of alleged malpractice with severe neurological injuries, the court took a restrictive interpretation of the PSQIA as it relates to Florida’s risk-management and discovery laws, holding that patient safety work and related reports, when required by state law, do not come under the definition of patient safety work product and were therefore discoverable.⁷

The Pennsylvania Supreme Court has likewise ruled that documents generated by a hospital’s outside contractor are not protected from discovery under the state’s Peer Review Protection Act. It agreed with a lower-court ruling that Monongahela Valley Hospital could not claim privilege for a performance file on an emergency department physician employed by the hospital’s contractor University of Pittsburgh Medical Center Emergency Medicine.⁸ The case alleged that the plaintiff’s chest and back pain was misdiagnosed as reflux disease when in fact it was a myocardial infarct.

Dr. Tan is professor of medicine and former adjunct professor of law at the University of Hawaii. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at siang@hawaii.edu.

References

1. Hawaii Revised Statutes §624-25.5 (2012).

2. AMA fights to protect patient-safety work from legal discovery. AMA Morning Rounds. 2018 Aug 1.
 

3. Daley v. Teruel and Ingalls Memorial Hospital, 2018 Ill. App. LEXIS 440 (Ill. App. Ct. 2018).

4. Brugaletta v. Garcia, 190 A.3d 419 (NJ. 2018).

5. Dwyer v. Ascension Crittenton Hospital. Michigan Supreme Court SC: 158668, 919 N.W.2d 407 (Mi. 2018).

6. Appellate court case puts peer-review protections in danger. AMA Morning Rounds. 2019 Mar 29.

7. Charles v. Southern Baptist Hospital of Florida, Inc., 2017 Fla. LEXIS 231 (Fla. Jan. 31, 2017).

8. Reginelli v. Boggs, 2018 Pa. LEXIS 1503 (Pa. 2018).

 

Question: A patient died unexpectedly during hospitalization for a diabetic foot infection. The autopsy revealed the presence of a large saddle pulmonary embolus. The hospital’s peer review committee met to determine if care was suboptimal and whether prophylactic anticoagulation should have been used. When the attending doctor was subsequently sued for malpractice, the plaintiff’s attorney sought to subpoena all of the medical records, including the minutes of the peer review committee. Given this hypothetical scenario, which of the following can occur?

A. “Discovery” is the legal term given to the process during the pretrial phase for amassing relevant documents and other information.

B. A subpoena duces tecum, which is a court order for the production of relevant documents and one that should normally be obeyed, may be issued.

C. The hospital declines to hand over certain types of hospital records, such as peer review minutes, which in this case are statutorily protected from discovery.

D. The plaintiff attorney goes to the judge for an order to compel production and may or may not be successful.

E. All are correct.
 

Answer: E. Physicians and other participants regularly meet, under strict confidential conditions, to discuss adverse events that occur in their institution. Congress and state legislatures have enacted laws to ensure the confidentiality of medical peer review, incident reports, and patient safety work products. Such records are protected from “discovery,” which is a pretrial procedure for collecting evidence in preparation for trial. The rationale for keeping these records beyond the reach of the discovery process is to encourage participants to engage in candid and free-rein analysis of adverse medical events so as to avoid future mishaps. If the content and nature of these discussions were freely available to parties in litigation, there would be a natural reluctance to express one’s viewpoints in a forthright manner.

Any given state’s statute on discovery requires careful reading because it could differ from another state’s directive – with important legal consequences. As an example, Hawaii’s statute¹ contains several inclusions and exclusions and reads in part: “... the information and data protected shall include proceedings and records of a peer review committee, hospital quality assurance committee, or health care review organization that include recordings, transcripts, minutes, and summaries of meetings, conversations, notes, materials, or reports created for, by, or at the direction of a peer review committee, quality assurance committee, or a health care review organization when related to a medical error reporting system. ... Information and data protected from discovery shall not include incident reports, occurrence reports, statements, or similar reports that state facts concerning a specific situation and shall not include records made in the regular course of business by a hospital ... including patient medical records. Original sources of information ... shall not be construed as being immune from discovery ... merely because they were reviewed ... or were in fact submitted to, a health care review organization.”

Predictably, plaintiff attorneys in a medical malpractice lawsuit will attempt to discover information regarding adverse events, hoping to learn about potential errors and judgment lapses, and thus gain an advantage over the defendant doctor and/or hospital. Several recent court cases highlight the contentious nature regarding whether a particular hospital report is to be deemed discoverable. Organized medicine, led by the American Medical Association, has mounted a vigorous response in arguing against the release of peer review and patient safety documents.

The AMA² recently weighed in on the case of Daley v. Teruel and Ingalls Memorial Hospital. In 2013, a renal failure patient died in an Illinois hospital from injuries that arose from prolonged hypoglycemia. She had received insulin, but when her blood glucose dropped to 16 mg/dl, the treatment team was not alerted and she was later found unresponsive with irreversible brain damage. The issue was whether incident reports from the case that were submitted to a certified PSO (patient safety organization) could be discovered. The Federal Patient Safety and Quality Improvement Act (PSQIA) had created PSOs to aggregate data from multiple sources to reduce adverse events and errors and improve medication safety.

An Illinois lower court ruled that, as part of the discovery process, the hospital had to turn over the report. However, the Illinois Appellate Court ruled in favor of the hospital, holding that the PSQIA protects the report because it is a “patient safety work product.”³ The AMA amicus brief had emphasized that Congress created a safeguarded patient safety process under the PSQIA to encourage hospitals to submit patient safety outcomes without fear of increased liability risk and that “these voluntarily created materials should be used for their intended purpose, not as a roadmap for litigation.”

New Jersey has also ruled against the discovery of a hospital’s self-critical report of a patient’s care, prepared in accordance with New Jersey’s Patient Safety Act.⁴ The plaintiff alleged that, when she reported to the emergency room at Chilton Medical Center complaining of persistent abdominal pain, fever, body aches, weakness, and a phlegmatic cough, she was incorrectly diagnosed as having pneumonia. In fact, she had appendicitis and a pelvic abscess. The New Jersey Supreme Court affirmed the panel’s order shielding the redacted document from discovery, but it reversed the judgment to the extent it ended the defendants’ discovery obligation with respect to this dispute, requiring instead that the lower court address, through current discovery rules, the proper balancing of interests between requesting and responding parties.

In a recent Michigan case,⁵ the trial court had earlier ruled that peer review documents at issue were in fact discoverable. Like similar statutes elsewhere, Michigan’s peer review privileges serve to encourage participation to improve on patient morbidity and mortality. The case centered on a court order compelling a Michigan hospital to release a physician’s credentialing file in a medical liability lawsuit on the narrow basis that the nondiscoverability privilege applied only to peer review deliberations and was inapplicable in the case. The trial judge had opined that, if all materials viewed by peer review committees were deemed undiscoverable, a hospital could never be held accountable for any negligent act within the purview of the committee. In its amicus brief in support of the hospital, the AMA argued that Michigan’s peer review privilege has historically spanned the bounds of the actual peer review process, and it countered that hospitals can be held liable – and are regularly held liable – without opening up these documents and that plaintiffs can use the same discovery mechanisms generally available to plaintiffs in other lawsuits.⁶ The case is currently under appeal.

In contrast, at least two state supreme courts have ruled to limit protections from discovery. The Florida Supreme Court has held that the federal law was intended to improve overall health care rather than to act as a shield to providers. In a case of alleged malpractice with severe neurological injuries, the court took a restrictive interpretation of the PSQIA as it relates to Florida’s risk-management and discovery laws, holding that patient safety work and related reports, when required by state law, do not come under the definition of patient safety work product and were therefore discoverable.⁷

The Pennsylvania Supreme Court has likewise ruled that documents generated by a hospital’s outside contractor are not protected from discovery under the state’s Peer Review Protection Act. It agreed with a lower-court ruling that Monongahela Valley Hospital could not claim privilege for a performance file on an emergency department physician employed by the hospital’s contractor University of Pittsburgh Medical Center Emergency Medicine.⁸ The case alleged that the plaintiff’s chest and back pain was misdiagnosed as reflux disease when in fact it was a myocardial infarct.

Dr. Tan is professor of medicine and former adjunct professor of law at the University of Hawaii. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at siang@hawaii.edu.

References

1. Hawaii Revised Statutes §624-25.5 (2012).

2. AMA fights to protect patient-safety work from legal discovery. AMA Morning Rounds. 2018 Aug 1.
 

3. Daley v. Teruel and Ingalls Memorial Hospital, 2018 Ill. App. LEXIS 440 (Ill. App. Ct. 2018).

4. Brugaletta v. Garcia, 190 A.3d 419 (NJ. 2018).

5. Dwyer v. Ascension Crittenton Hospital. Michigan Supreme Court SC: 158668, 919 N.W.2d 407 (Mi. 2018).

6. Appellate court case puts peer-review protections in danger. AMA Morning Rounds. 2019 Mar 29.

7. Charles v. Southern Baptist Hospital of Florida, Inc., 2017 Fla. LEXIS 231 (Fla. Jan. 31, 2017).

8. Reginelli v. Boggs, 2018 Pa. LEXIS 1503 (Pa. 2018).

 

Question: A patient died unexpectedly during hospitalization for a diabetic foot infection. The autopsy revealed the presence of a large saddle pulmonary embolus. The hospital’s peer review committee met to determine if care was suboptimal and whether prophylactic anticoagulation should have been used. When the attending doctor was subsequently sued for malpractice, the plaintiff’s attorney sought to subpoena all of the medical records, including the minutes of the peer review committee. Given this hypothetical scenario, which of the following can occur?

A. “Discovery” is the legal term given to the process during the pretrial phase for amassing relevant documents and other information.

B. A subpoena duces tecum, which is a court order for the production of relevant documents and one that should normally be obeyed, may be issued.

C. The hospital declines to hand over certain types of hospital records, such as peer review minutes, which in this case are statutorily protected from discovery.

D. The plaintiff attorney goes to the judge for an order to compel production and may or may not be successful.

E. All are correct.
 

Answer: E. Physicians and other participants regularly meet, under strict confidential conditions, to discuss adverse events that occur in their institution. Congress and state legislatures have enacted laws to ensure the confidentiality of medical peer review, incident reports, and patient safety work products. Such records are protected from “discovery,” which is a pretrial procedure for collecting evidence in preparation for trial. The rationale for keeping these records beyond the reach of the discovery process is to encourage participants to engage in candid and free-rein analysis of adverse medical events so as to avoid future mishaps. If the content and nature of these discussions were freely available to parties in litigation, there would be a natural reluctance to express one’s viewpoints in a forthright manner.

Any given state’s statute on discovery requires careful reading because it could differ from another state’s directive – with important legal consequences. As an example, Hawaii’s statute¹ contains several inclusions and exclusions and reads in part: “... the information and data protected shall include proceedings and records of a peer review committee, hospital quality assurance committee, or health care review organization that include recordings, transcripts, minutes, and summaries of meetings, conversations, notes, materials, or reports created for, by, or at the direction of a peer review committee, quality assurance committee, or a health care review organization when related to a medical error reporting system. ... Information and data protected from discovery shall not include incident reports, occurrence reports, statements, or similar reports that state facts concerning a specific situation and shall not include records made in the regular course of business by a hospital ... including patient medical records. Original sources of information ... shall not be construed as being immune from discovery ... merely because they were reviewed ... or were in fact submitted to, a health care review organization.”

Predictably, plaintiff attorneys in a medical malpractice lawsuit will attempt to discover information regarding adverse events, hoping to learn about potential errors and judgment lapses, and thus gain an advantage over the defendant doctor and/or hospital. Several recent court cases highlight the contentious nature regarding whether a particular hospital report is to be deemed discoverable. Organized medicine, led by the American Medical Association, has mounted a vigorous response in arguing against the release of peer review and patient safety documents.

The AMA² recently weighed in on the case of Daley v. Teruel and Ingalls Memorial Hospital. In 2013, a renal failure patient died in an Illinois hospital from injuries that arose from prolonged hypoglycemia. She had received insulin, but when her blood glucose dropped to 16 mg/dl, the treatment team was not alerted and she was later found unresponsive with irreversible brain damage. The issue was whether incident reports from the case that were submitted to a certified PSO (patient safety organization) could be discovered. The Federal Patient Safety and Quality Improvement Act (PSQIA) had created PSOs to aggregate data from multiple sources to reduce adverse events and errors and improve medication safety.

An Illinois lower court ruled that, as part of the discovery process, the hospital had to turn over the report. However, the Illinois Appellate Court ruled in favor of the hospital, holding that the PSQIA protects the report because it is a “patient safety work product.”³ The AMA amicus brief had emphasized that Congress created a safeguarded patient safety process under the PSQIA to encourage hospitals to submit patient safety outcomes without fear of increased liability risk and that “these voluntarily created materials should be used for their intended purpose, not as a roadmap for litigation.”

New Jersey has also ruled against the discovery of a hospital’s self-critical report of a patient’s care, prepared in accordance with New Jersey’s Patient Safety Act.⁴ The plaintiff alleged that, when she reported to the emergency room at Chilton Medical Center complaining of persistent abdominal pain, fever, body aches, weakness, and a phlegmatic cough, she was incorrectly diagnosed as having pneumonia. In fact, she had appendicitis and a pelvic abscess. The New Jersey Supreme Court affirmed the panel’s order shielding the redacted document from discovery, but it reversed the judgment to the extent it ended the defendants’ discovery obligation with respect to this dispute, requiring instead that the lower court address, through current discovery rules, the proper balancing of interests between requesting and responding parties.

In a recent Michigan case,⁵ the trial court had earlier ruled that peer review documents at issue were in fact discoverable. Like similar statutes elsewhere, Michigan’s peer review privileges serve to encourage participation to improve on patient morbidity and mortality. The case centered on a court order compelling a Michigan hospital to release a physician’s credentialing file in a medical liability lawsuit on the narrow basis that the nondiscoverability privilege applied only to peer review deliberations and was inapplicable in the case. The trial judge had opined that, if all materials viewed by peer review committees were deemed undiscoverable, a hospital could never be held accountable for any negligent act within the purview of the committee. In its amicus brief in support of the hospital, the AMA argued that Michigan’s peer review privilege has historically spanned the bounds of the actual peer review process, and it countered that hospitals can be held liable – and are regularly held liable – without opening up these documents and that plaintiffs can use the same discovery mechanisms generally available to plaintiffs in other lawsuits.⁶ The case is currently under appeal.

In contrast, at least two state supreme courts have ruled to limit protections from discovery. The Florida Supreme Court has held that the federal law was intended to improve overall health care rather than to act as a shield to providers. In a case of alleged malpractice with severe neurological injuries, the court took a restrictive interpretation of the PSQIA as it relates to Florida’s risk-management and discovery laws, holding that patient safety work and related reports, when required by state law, do not come under the definition of patient safety work product and were therefore discoverable.⁷

The Pennsylvania Supreme Court has likewise ruled that documents generated by a hospital’s outside contractor are not protected from discovery under the state’s Peer Review Protection Act. It agreed with a lower-court ruling that Monongahela Valley Hospital could not claim privilege for a performance file on an emergency department physician employed by the hospital’s contractor University of Pittsburgh Medical Center Emergency Medicine.⁸ The case alleged that the plaintiff’s chest and back pain was misdiagnosed as reflux disease when in fact it was a myocardial infarct.

Dr. Tan is professor of medicine and former adjunct professor of law at the University of Hawaii. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at siang@hawaii.edu.

References

1. Hawaii Revised Statutes §624-25.5 (2012).

2. AMA fights to protect patient-safety work from legal discovery. AMA Morning Rounds. 2018 Aug 1.
 

3. Daley v. Teruel and Ingalls Memorial Hospital, 2018 Ill. App. LEXIS 440 (Ill. App. Ct. 2018).

4. Brugaletta v. Garcia, 190 A.3d 419 (NJ. 2018).

5. Dwyer v. Ascension Crittenton Hospital. Michigan Supreme Court SC: 158668, 919 N.W.2d 407 (Mi. 2018).

6. Appellate court case puts peer-review protections in danger. AMA Morning Rounds. 2019 Mar 29.

7. Charles v. Southern Baptist Hospital of Florida, Inc., 2017 Fla. LEXIS 231 (Fla. Jan. 31, 2017).

8. Reginelli v. Boggs, 2018 Pa. LEXIS 1503 (Pa. 2018).

 

My grandfather used to say: “Son, keep your powder dry.” The old aphorism is basically a reminder to keep your power or influence in reserve until you really need it. In my case, he could simply have been trying to quiet an overly talkative kid. But anything my grandfather said that had to do with guns carried great authority with me. He owned a shotgun that had been converted from a flintlock by his grandfather, and we grandchildren were schooled in its use.

I was recently reminded of my grandfather’s advice as I was about to participate in a planned meeting. One of the meeting leaders pulled me aside to tell me that I was not to ask questions, and informed me that if I did ask questions, I would be punished to the fullest extent possible. I also was not to challenge the preordained conclusion.

I was simultaneously aghast and impressed. Never had I heard such a trifecta of terrible leadership uttered in a single breath. It was a reminder to revisit the premises of all the books I had read and the conferences I had attended on leadership.

There are basic prerequisites of building consensus and adopting new ideas.

First, you must introduce the wonderful idea and explain it to everyone. It is even better when you are able to back up someone else’s great idea.

Next, you must allow the group to discuss the idea and be open to change. This may involve shelving, or even killing, your shiny new idea.

You must allow time for things to sink in regarding the idea. If you want something to stick, people have to adapt and adopt. If your idea is truly wonderful, you should be able to attract advocates and get a majority to agree to the plan. You should make sure they get to vote on the plan. If you lose the vote, don’t try any maneuvers to undo your loss. Accept it and move on. If your idea is good, it will surface again as someone else’s idea and be a much easier pitch.

Finally, never, ever bully or threaten. Memories are long, and while some may not agree with your idea, they won’t actively try to kill it later or undermine future projects. Pinch yourself every day, and remember that you are a servant of the group. You are a facilitator, not an autocrat.

That said, leaders differ in their styles of leadership. I think the best leaders are not afraid to listen to their boards and membership. Their actions focus thoughts and move things along. If you let your board members own their actions, they will respect you. You will build up tremendous goodwill (and powder). With any luck, you may never need to draw on this goodwill; but if there is a crisis and you need to put a bullet through something quickly, your intentions will not be questioned. At a minimum, you will have plenty of opportunity to explain your actions.

So it saddens me to see leaders burn all their powder and lose their influence. It’s not good for them or their organization, and they will likely have to overcome unexpected resistance in the future.

Leaders, keep your powder dry!

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Dr. Coldiron is the chair of SkinPAC for 2019-2021; this is an unpaid volunteer position. Write to him at dermnews@mdedge.com.

 

My grandfather used to say: “Son, keep your powder dry.” The old aphorism is basically a reminder to keep your power or influence in reserve until you really need it. In my case, he could simply have been trying to quiet an overly talkative kid. But anything my grandfather said that had to do with guns carried great authority with me. He owned a shotgun that had been converted from a flintlock by his grandfather, and we grandchildren were schooled in its use.

I was recently reminded of my grandfather’s advice as I was about to participate in a planned meeting. One of the meeting leaders pulled me aside to tell me that I was not to ask questions, and informed me that if I did ask questions, I would be punished to the fullest extent possible. I also was not to challenge the preordained conclusion.

I was simultaneously aghast and impressed. Never had I heard such a trifecta of terrible leadership uttered in a single breath. It was a reminder to revisit the premises of all the books I had read and the conferences I had attended on leadership.

There are basic prerequisites of building consensus and adopting new ideas.

First, you must introduce the wonderful idea and explain it to everyone. It is even better when you are able to back up someone else’s great idea.

Next, you must allow the group to discuss the idea and be open to change. This may involve shelving, or even killing, your shiny new idea.

You must allow time for things to sink in regarding the idea. If you want something to stick, people have to adapt and adopt. If your idea is truly wonderful, you should be able to attract advocates and get a majority to agree to the plan. You should make sure they get to vote on the plan. If you lose the vote, don’t try any maneuvers to undo your loss. Accept it and move on. If your idea is good, it will surface again as someone else’s idea and be a much easier pitch.

Finally, never, ever bully or threaten. Memories are long, and while some may not agree with your idea, they won’t actively try to kill it later or undermine future projects. Pinch yourself every day, and remember that you are a servant of the group. You are a facilitator, not an autocrat.

That said, leaders differ in their styles of leadership. I think the best leaders are not afraid to listen to their boards and membership. Their actions focus thoughts and move things along. If you let your board members own their actions, they will respect you. You will build up tremendous goodwill (and powder). With any luck, you may never need to draw on this goodwill; but if there is a crisis and you need to put a bullet through something quickly, your intentions will not be questioned. At a minimum, you will have plenty of opportunity to explain your actions.

So it saddens me to see leaders burn all their powder and lose their influence. It’s not good for them or their organization, and they will likely have to overcome unexpected resistance in the future.

Leaders, keep your powder dry!

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Dr. Coldiron is the chair of SkinPAC for 2019-2021; this is an unpaid volunteer position. Write to him at dermnews@mdedge.com.

 

My grandfather used to say: “Son, keep your powder dry.” The old aphorism is basically a reminder to keep your power or influence in reserve until you really need it. In my case, he could simply have been trying to quiet an overly talkative kid. But anything my grandfather said that had to do with guns carried great authority with me. He owned a shotgun that had been converted from a flintlock by his grandfather, and we grandchildren were schooled in its use.

I was recently reminded of my grandfather’s advice as I was about to participate in a planned meeting. One of the meeting leaders pulled me aside to tell me that I was not to ask questions, and informed me that if I did ask questions, I would be punished to the fullest extent possible. I also was not to challenge the preordained conclusion.

I was simultaneously aghast and impressed. Never had I heard such a trifecta of terrible leadership uttered in a single breath. It was a reminder to revisit the premises of all the books I had read and the conferences I had attended on leadership.

There are basic prerequisites of building consensus and adopting new ideas.

First, you must introduce the wonderful idea and explain it to everyone. It is even better when you are able to back up someone else’s great idea.

Next, you must allow the group to discuss the idea and be open to change. This may involve shelving, or even killing, your shiny new idea.

You must allow time for things to sink in regarding the idea. If you want something to stick, people have to adapt and adopt. If your idea is truly wonderful, you should be able to attract advocates and get a majority to agree to the plan. You should make sure they get to vote on the plan. If you lose the vote, don’t try any maneuvers to undo your loss. Accept it and move on. If your idea is good, it will surface again as someone else’s idea and be a much easier pitch.

Finally, never, ever bully or threaten. Memories are long, and while some may not agree with your idea, they won’t actively try to kill it later or undermine future projects. Pinch yourself every day, and remember that you are a servant of the group. You are a facilitator, not an autocrat.

That said, leaders differ in their styles of leadership. I think the best leaders are not afraid to listen to their boards and membership. Their actions focus thoughts and move things along. If you let your board members own their actions, they will respect you. You will build up tremendous goodwill (and powder). With any luck, you may never need to draw on this goodwill; but if there is a crisis and you need to put a bullet through something quickly, your intentions will not be questioned. At a minimum, you will have plenty of opportunity to explain your actions.

So it saddens me to see leaders burn all their powder and lose their influence. It’s not good for them or their organization, and they will likely have to overcome unexpected resistance in the future.

Leaders, keep your powder dry!

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Dr. Coldiron is the chair of SkinPAC for 2019-2021; this is an unpaid volunteer position. Write to him at dermnews@mdedge.com.

 

When you fly as a physician, there’s always a chance you’ll get a free drink. It’s not free, of course. For at least a few minutes, you worked. “Is there a physician onboard? – Ah, just how badly do you want that vodka tonic?

I ring my call button, as I’m sure you do. (It’s worth it to see the flight attendant’s face when I reply: “I’m a dermatologist.”) Last time it was for a 68-year-old man who was vomiting. There was no rash.

I responded along with a pediatrician and an ER nurse – gratitude is an ER nurse at 38,000 feet. The patient had chemotherapy-induced nausea. We three managed to get him well enough to finish the flight. Our ER nurse team member ran the show; she was excellent. She asked all the right questions and helped us all make good decisions. Unlike in clinic, I wasn’t an expert here despite my MD.

Several weeks ago, I saw a patient in the office with severe psoriasis. She stood before me erythrodermic. As I was adjusting her orders, I stepped out of the office to call one of my partners for her opinion. She examined the patient and declared: “I don’t think it’s psoriasis. Despite that biopsy, I think this is chronic eczema.” Brilliant.

In contrast to the former story, I was an expert in my office. And yet, success depended in both instances on my recognizing a cognitive bias: I don’t know everything, and worse, I sometimes don’t realize what I don’t know.

There are several biases of overconfidence. One is the expert trap: You believe you are an expert or correct, but you are wrong and you don’t see it. It’s a common mistake and manifests as overconfidence in our own abilities. For example, what decade did Hawaii join the union? Who is on the 20-dollar bill? Which is the farthest planet? You might be 90% confident of your answers, but most of us are more confident than we ought to be. Chances are you’ll be wrong on one. Recognizing this is hard. And yet, it’s what separates the good from the great clinicians.

Short of having your medical assistant whisper in your ear each day “Memento stultus” (remember you’re stupid), avoiding this bias is difficult. Signs that you might be trapped in an expert mindset are: 1. You believe your patients’ failure to improve is due to lack of adherence to your plan. 2. You cannot recall the last time you tried a new treatment. 3. You never ask others for second opinions. 4. Your colleagues stop asking for your opinion. 5. A flight attendant asks if you would mind returning to your seat rather than help with a medical situation.

If you want to be a better doctor, try working on your sense of self-importance. Remember your limitations and those of medicine. Be methodical in questioning your assumptions. Could you be wrong? Could the data you have be misleading? What are you missing? Ask a colleague to review some of your charts or spend time with you during procedures. Join (or start!) a journal club. Share your difficult cases with others and take note of how their advice differs from your approach.

By recognizing when you might be wrong and humbly stepping aside or taking the time to learn, you might just earn that free drink.

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

 

When you fly as a physician, there’s always a chance you’ll get a free drink. It’s not free, of course. For at least a few minutes, you worked. “Is there a physician onboard? – Ah, just how badly do you want that vodka tonic?

I ring my call button, as I’m sure you do. (It’s worth it to see the flight attendant’s face when I reply: “I’m a dermatologist.”) Last time it was for a 68-year-old man who was vomiting. There was no rash.

I responded along with a pediatrician and an ER nurse – gratitude is an ER nurse at 38,000 feet. The patient had chemotherapy-induced nausea. We three managed to get him well enough to finish the flight. Our ER nurse team member ran the show; she was excellent. She asked all the right questions and helped us all make good decisions. Unlike in clinic, I wasn’t an expert here despite my MD.

Several weeks ago, I saw a patient in the office with severe psoriasis. She stood before me erythrodermic. As I was adjusting her orders, I stepped out of the office to call one of my partners for her opinion. She examined the patient and declared: “I don’t think it’s psoriasis. Despite that biopsy, I think this is chronic eczema.” Brilliant.

In contrast to the former story, I was an expert in my office. And yet, success depended in both instances on my recognizing a cognitive bias: I don’t know everything, and worse, I sometimes don’t realize what I don’t know.

There are several biases of overconfidence. One is the expert trap: You believe you are an expert or correct, but you are wrong and you don’t see it. It’s a common mistake and manifests as overconfidence in our own abilities. For example, what decade did Hawaii join the union? Who is on the 20-dollar bill? Which is the farthest planet? You might be 90% confident of your answers, but most of us are more confident than we ought to be. Chances are you’ll be wrong on one. Recognizing this is hard. And yet, it’s what separates the good from the great clinicians.

Short of having your medical assistant whisper in your ear each day “Memento stultus” (remember you’re stupid), avoiding this bias is difficult. Signs that you might be trapped in an expert mindset are: 1. You believe your patients’ failure to improve is due to lack of adherence to your plan. 2. You cannot recall the last time you tried a new treatment. 3. You never ask others for second opinions. 4. Your colleagues stop asking for your opinion. 5. A flight attendant asks if you would mind returning to your seat rather than help with a medical situation.

If you want to be a better doctor, try working on your sense of self-importance. Remember your limitations and those of medicine. Be methodical in questioning your assumptions. Could you be wrong? Could the data you have be misleading? What are you missing? Ask a colleague to review some of your charts or spend time with you during procedures. Join (or start!) a journal club. Share your difficult cases with others and take note of how their advice differs from your approach.

By recognizing when you might be wrong and humbly stepping aside or taking the time to learn, you might just earn that free drink.

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

 

When you fly as a physician, there’s always a chance you’ll get a free drink. It’s not free, of course. For at least a few minutes, you worked. “Is there a physician onboard? – Ah, just how badly do you want that vodka tonic?

I ring my call button, as I’m sure you do. (It’s worth it to see the flight attendant’s face when I reply: “I’m a dermatologist.”) Last time it was for a 68-year-old man who was vomiting. There was no rash.

I responded along with a pediatrician and an ER nurse – gratitude is an ER nurse at 38,000 feet. The patient had chemotherapy-induced nausea. We three managed to get him well enough to finish the flight. Our ER nurse team member ran the show; she was excellent. She asked all the right questions and helped us all make good decisions. Unlike in clinic, I wasn’t an expert here despite my MD.

Several weeks ago, I saw a patient in the office with severe psoriasis. She stood before me erythrodermic. As I was adjusting her orders, I stepped out of the office to call one of my partners for her opinion. She examined the patient and declared: “I don’t think it’s psoriasis. Despite that biopsy, I think this is chronic eczema.” Brilliant.

In contrast to the former story, I was an expert in my office. And yet, success depended in both instances on my recognizing a cognitive bias: I don’t know everything, and worse, I sometimes don’t realize what I don’t know.

There are several biases of overconfidence. One is the expert trap: You believe you are an expert or correct, but you are wrong and you don’t see it. It’s a common mistake and manifests as overconfidence in our own abilities. For example, what decade did Hawaii join the union? Who is on the 20-dollar bill? Which is the farthest planet? You might be 90% confident of your answers, but most of us are more confident than we ought to be. Chances are you’ll be wrong on one. Recognizing this is hard. And yet, it’s what separates the good from the great clinicians.

Short of having your medical assistant whisper in your ear each day “Memento stultus” (remember you’re stupid), avoiding this bias is difficult. Signs that you might be trapped in an expert mindset are: 1. You believe your patients’ failure to improve is due to lack of adherence to your plan. 2. You cannot recall the last time you tried a new treatment. 3. You never ask others for second opinions. 4. Your colleagues stop asking for your opinion. 5. A flight attendant asks if you would mind returning to your seat rather than help with a medical situation.

If you want to be a better doctor, try working on your sense of self-importance. Remember your limitations and those of medicine. Be methodical in questioning your assumptions. Could you be wrong? Could the data you have be misleading? What are you missing? Ask a colleague to review some of your charts or spend time with you during procedures. Join (or start!) a journal club. Share your difficult cases with others and take note of how their advice differs from your approach.

By recognizing when you might be wrong and humbly stepping aside or taking the time to learn, you might just earn that free drink.

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

 

Parabens were named nonallergen of the year! It is time that we help consumers understand that the substitutes for parabens are often worse than parabens, and parabens are not as sensitizing as we thought. Preservatives are essential parts of most cosmetics and cosmeceuticals. (I say “most” because many organic products do not have them and consequently have shorter shelf lives.) Without them, products are vulnerable to rapid decomposition and infiltration by bacteria, fungi, and molds. The preservatives that are used in the place of parabens often are sensitizers. What do we tell our patients about the safety of parabens with all of these conflicting reports? This column will focus on current thoughts regarding the safety of parabens used as preservatives. I would love to hear your thoughts.

Background

monticelllo/iStock/Getty Images Plus

Parabens are alkyl esters of p-hydroxybenzoic acid and have been used as a class of preservatives since the late 1920s and early 1930s. Parabens are found naturally in raspberries, blackberries, carrots, and cucumbers and are common ingredients in food and pharmaceuticals. They are still widely used in skin, hair, and body care products, despite the public outcry against them.^1-4

There are many kinds of parabens such as butylparaben, isobutylparaben, ethylparaben, methylparaben, propylparaben, isopropylparaben, and benzylparaben, each with its own characteristics.⁵ Parabens are considered ideal preservative ingredients because they exhibit a broad spectrum of antimicrobial activity, stability over a large pH and temperature range, have no odor, do not change color, and are water soluble enough to yield an effective concentration in a hydrophilic formulation.³ As the alkyl chain length of parabens increases, they become less water soluble and more oil soluble. Parabens penetrate the skin barrier in inverse relation to its ester chain length.⁶ Often, several parabens will be combined to take advantage of each paraben’s solubility characteristics.

Many patients avoid parabens because of “health risks.” Now other preservatives are being substituted for parabens, even though these ingredients may be less studied or even less safe than parabens. It is important not to lump all parabens together as they each have different characteristics. Methylparaben and propylparaben are the most commonly used parabens in skin care products.⁷ Combinations of parabens are notably more effective than the use of single parabens.^3,8 High concentrations of any type of paraben can cause an irritant reaction on the skin, but those with longer ester chain lengths are more likely to cause irritation.

Methylparaben

The methyl ester of p-hydroxybenzoic acid is found in many skin care products. It is readily absorbed through the skin and gastrointestinal tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body. Studies have shown it is nontoxic, nonirritating, and nonsensitizing. It is not teratogenic, embryotoxic, or carcinogenic. Methylparaben, because of its shorter side chain groups and greater lipophilicity, has been shown to be more readily absorbed by the skin than other paraben chemicals.^8,9 It is also on the low order of ingredients provoking acute and chronic toxicity.³

 

Propylparaben

Propylparaben is the ester form of p-hydroxybenzoic acid that has been esterified with n-propanol. It is the most commonly used antimicrobial preservative in foods, cosmetics, and drugs. It is readily absorbed through the skin and GI tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body.

Estrogenic activity of parabens

In a 2004 study, Darbre et al. reported on the discovery of parabens-like substances in breast tissue and published these findings in the Journal of Applied Toxicology.¹⁰ The media and public panicked, saying that parabens have estrogenic activity and can cause breast cancer. However, many studies have shown that certain parabens do not have estrogenic activity. Although some parabens have been shown to impart estrogenic effects in vitro, these are very weak. The four most commonly used parabens in cosmetic products are 10,000-fold or less potent than 17beta-estradiol.¹¹ The potential to result in an adverse effect mediated via an estrogen mode of action has not been established in humans.⁶ Paraben exposure differs geographically. No correlation has been found between the amount of parabens in a geographic location and the incidence of breast cancer. Current scientific knowledge is insufficient to demonstrate a clear cancer risk caused by the topical application of cosmetics that contain parabens on normal intact skin.¹¹

Parabens and contact dermatitis

Paraben compounds are capable of minimal penetrance through intact skin.¹² When they are able to penetrate the skin – a capacity that varies among the class – parabens are rapidly metabolized to p-hydroxybenzoic acid and promptly excreted in the urine.^3,11 Parabens for many years were thought to cause contact dermatitis, and there are many reports of this. However, the incidence is much lower than previously thought. In fact, parabens were named “Nonallergen of the Year in 2018” because of the low incidence of reactions in patch tests.¹³ Higher concentrations of parabens applied topically to skin – especially “nonintact” skin – have been shown to cause mild irritant reactions. It is likely that many of these reported cases of “contact dermatitis” were actually irritant dermatitis. Longstanding concerns about the allergenicity of parabens in relation to the skin have been rendered insignificant, as the wealth of evidence reveals little to no support for the cutaneous toxicity of these substances.¹¹ Yim et al. add that parabens remain far less sensitizing than agents newly introduced for use in personal care products.⁴

Daily average exposure to parabens

It is estimated that parabens are found in 10% of personal care products. In most cases, these products contain 1% or less of parabens. If the average patient uses 50 g of personal care products a day, then the average daily exposure to parabens topically is 0.05 g. Parabens also are found in food and drugs, so the total paraben exposure per day is assumed to be about 1 mg/day. (See the 2002 Food and Chemical Toxicology article for details of how this was calculated.)⁷ When food, personal care products, and drug exposure rates are added, the average person is exposed to 1.29 mg/kg per day or 77.5 mg/day for a 60-kg individual. You can see that personal care products account for a fraction of exposure, as most paraben exposure comes from food.

 

Government opinion on the safety of parabens for the skin

Parabens long have been assessed as safe for use in cosmetic products in many countries. The European Commission stipulated a maximum concentration of 0.4% for each paraben and 0.8% for total mixture of paraben esters.^4,6 While the Federal Food, Drug, and Cosmetic Act of 1938 prohibits the Food and Drug Administration from ruling on cosmetic ingredients, the industry-sponsored Cosmetic Ingredient Review expert panel has endorsed the European guidelines.^4,6 Further, the North American Contact Dermatitis Group has pointed out that parabens continue to demonstrate the lowest prevalence of positivity (0.6%) of any major preservative available on the North American market, which includes over 10,000 cosmetic and personal care products, and remain one of the safest classes of preservatives for the skin.¹⁴ Further, the FDA has listed or classified parabens as generally regarded as safe.⁸

Safety of parabens

Parabens do not accumulate in tissues or organs for any appreciable length of time.^6,8 In addition, carcinogenicity, cytotoxicity, or mutagenicity has not been proven in relation to parabens.⁸ Indeed, classical assays have shown no activity from parabens in terms of mutagenicity or carcinogenicity.^11,15 Some estrogenic effects or activity that mimics estrogen have been associated with parabens in vitro, but this activity has been noted as very weak and there are no established reports of human cases in which parabens have elicited an estrogen-mediated adverse event.^6,11

Concerns about a possible link between parabens and breast cancer have been largely diminished or relegated to the status of unknown and difficult to ascertain.¹³ Further, present knowledge provides no established link between the topical application of parabens-containing skin care formulations on healthy skin and cancer risk.¹⁰ Only intact skin should come in touch with products containing parabens to prevent irritant reactions.

Conclusion

Despite the fearful hype and reaction to one report 15 years ago, parabens continue to be safely used in numerous topical formulations. Their widespread use and lack of association with adverse events are a testament to their safety. There are no data to support discouraging patients from using parabens-containing products, which often are safer than other preservative alternatives. From a dermatologic perspective, this nonallergen of the year deserves a better reputation.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems. Write to her at dermnews@mdedge.com

References

1. “Goodman and Gilman’s The Pharmacological Basis of Therapeutics,” 6th ed. (New York: Macmillan, 1980, p. 969).

2. Toxicity: The Butyl, Ethyl, Methyl, and Propyl Esters have been found to promote allergic sensitization in humans, in “Dangerous Properties of Industrial Materials,” 4th ed. (New York: Van Nostrand Reinhold, 1975, p. 929).

3. Food Chem Toxicol. 2001 Jun;39(6):513-32.

4. Dermatitis. 2014 Sep-Oct;25(5):215-31.

5. Crit Rev Toxicol. 2005 Jun;35(5):435-58.

6. Int J Toxicol. 2008;27 Suppl 4:1-82.

7. Food Chem Toxicol. 2002 Oct;40(10):1335-73.

8. Dermatitis. 2019 Jan/Feb;30(1):3-31.

9. Exp Dermatol. 2007 Oct;16(10):830-6.

10. J Appl Toxicol. 2004 Jan-Feb;24(1):5-13.

11. Dermatitis. 2019 Jan/Feb;30(1):32-45.

12. Food Chem Toxicol. 2005 Feb;43(2):279-91.

13. Dermatitis. 2018 Dec 18. doi: 10.1097/DER.0000000000000429.

14. Dermatitis. 2018 Nov/Dec;29(6):297-309.

15. Food Chem Toxicol. 2005 Jul;43(7):985-1015.

 

Parabens were named nonallergen of the year! It is time that we help consumers understand that the substitutes for parabens are often worse than parabens, and parabens are not as sensitizing as we thought. Preservatives are essential parts of most cosmetics and cosmeceuticals. (I say “most” because many organic products do not have them and consequently have shorter shelf lives.) Without them, products are vulnerable to rapid decomposition and infiltration by bacteria, fungi, and molds. The preservatives that are used in the place of parabens often are sensitizers. What do we tell our patients about the safety of parabens with all of these conflicting reports? This column will focus on current thoughts regarding the safety of parabens used as preservatives. I would love to hear your thoughts.

Background

monticelllo/iStock/Getty Images Plus

Parabens are alkyl esters of p-hydroxybenzoic acid and have been used as a class of preservatives since the late 1920s and early 1930s. Parabens are found naturally in raspberries, blackberries, carrots, and cucumbers and are common ingredients in food and pharmaceuticals. They are still widely used in skin, hair, and body care products, despite the public outcry against them.^1-4

There are many kinds of parabens such as butylparaben, isobutylparaben, ethylparaben, methylparaben, propylparaben, isopropylparaben, and benzylparaben, each with its own characteristics.⁵ Parabens are considered ideal preservative ingredients because they exhibit a broad spectrum of antimicrobial activity, stability over a large pH and temperature range, have no odor, do not change color, and are water soluble enough to yield an effective concentration in a hydrophilic formulation.³ As the alkyl chain length of parabens increases, they become less water soluble and more oil soluble. Parabens penetrate the skin barrier in inverse relation to its ester chain length.⁶ Often, several parabens will be combined to take advantage of each paraben’s solubility characteristics.

Many patients avoid parabens because of “health risks.” Now other preservatives are being substituted for parabens, even though these ingredients may be less studied or even less safe than parabens. It is important not to lump all parabens together as they each have different characteristics. Methylparaben and propylparaben are the most commonly used parabens in skin care products.⁷ Combinations of parabens are notably more effective than the use of single parabens.^3,8 High concentrations of any type of paraben can cause an irritant reaction on the skin, but those with longer ester chain lengths are more likely to cause irritation.

Methylparaben

The methyl ester of p-hydroxybenzoic acid is found in many skin care products. It is readily absorbed through the skin and gastrointestinal tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body. Studies have shown it is nontoxic, nonirritating, and nonsensitizing. It is not teratogenic, embryotoxic, or carcinogenic. Methylparaben, because of its shorter side chain groups and greater lipophilicity, has been shown to be more readily absorbed by the skin than other paraben chemicals.^8,9 It is also on the low order of ingredients provoking acute and chronic toxicity.³

 

Propylparaben

Propylparaben is the ester form of p-hydroxybenzoic acid that has been esterified with n-propanol. It is the most commonly used antimicrobial preservative in foods, cosmetics, and drugs. It is readily absorbed through the skin and GI tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body.

Estrogenic activity of parabens

In a 2004 study, Darbre et al. reported on the discovery of parabens-like substances in breast tissue and published these findings in the Journal of Applied Toxicology.¹⁰ The media and public panicked, saying that parabens have estrogenic activity and can cause breast cancer. However, many studies have shown that certain parabens do not have estrogenic activity. Although some parabens have been shown to impart estrogenic effects in vitro, these are very weak. The four most commonly used parabens in cosmetic products are 10,000-fold or less potent than 17beta-estradiol.¹¹ The potential to result in an adverse effect mediated via an estrogen mode of action has not been established in humans.⁶ Paraben exposure differs geographically. No correlation has been found between the amount of parabens in a geographic location and the incidence of breast cancer. Current scientific knowledge is insufficient to demonstrate a clear cancer risk caused by the topical application of cosmetics that contain parabens on normal intact skin.¹¹

Parabens and contact dermatitis

Paraben compounds are capable of minimal penetrance through intact skin.¹² When they are able to penetrate the skin – a capacity that varies among the class – parabens are rapidly metabolized to p-hydroxybenzoic acid and promptly excreted in the urine.^3,11 Parabens for many years were thought to cause contact dermatitis, and there are many reports of this. However, the incidence is much lower than previously thought. In fact, parabens were named “Nonallergen of the Year in 2018” because of the low incidence of reactions in patch tests.¹³ Higher concentrations of parabens applied topically to skin – especially “nonintact” skin – have been shown to cause mild irritant reactions. It is likely that many of these reported cases of “contact dermatitis” were actually irritant dermatitis. Longstanding concerns about the allergenicity of parabens in relation to the skin have been rendered insignificant, as the wealth of evidence reveals little to no support for the cutaneous toxicity of these substances.¹¹ Yim et al. add that parabens remain far less sensitizing than agents newly introduced for use in personal care products.⁴

Daily average exposure to parabens

It is estimated that parabens are found in 10% of personal care products. In most cases, these products contain 1% or less of parabens. If the average patient uses 50 g of personal care products a day, then the average daily exposure to parabens topically is 0.05 g. Parabens also are found in food and drugs, so the total paraben exposure per day is assumed to be about 1 mg/day. (See the 2002 Food and Chemical Toxicology article for details of how this was calculated.)⁷ When food, personal care products, and drug exposure rates are added, the average person is exposed to 1.29 mg/kg per day or 77.5 mg/day for a 60-kg individual. You can see that personal care products account for a fraction of exposure, as most paraben exposure comes from food.

 

Government opinion on the safety of parabens for the skin

Parabens long have been assessed as safe for use in cosmetic products in many countries. The European Commission stipulated a maximum concentration of 0.4% for each paraben and 0.8% for total mixture of paraben esters.^4,6 While the Federal Food, Drug, and Cosmetic Act of 1938 prohibits the Food and Drug Administration from ruling on cosmetic ingredients, the industry-sponsored Cosmetic Ingredient Review expert panel has endorsed the European guidelines.^4,6 Further, the North American Contact Dermatitis Group has pointed out that parabens continue to demonstrate the lowest prevalence of positivity (0.6%) of any major preservative available on the North American market, which includes over 10,000 cosmetic and personal care products, and remain one of the safest classes of preservatives for the skin.¹⁴ Further, the FDA has listed or classified parabens as generally regarded as safe.⁸

Safety of parabens

Parabens do not accumulate in tissues or organs for any appreciable length of time.^6,8 In addition, carcinogenicity, cytotoxicity, or mutagenicity has not been proven in relation to parabens.⁸ Indeed, classical assays have shown no activity from parabens in terms of mutagenicity or carcinogenicity.^11,15 Some estrogenic effects or activity that mimics estrogen have been associated with parabens in vitro, but this activity has been noted as very weak and there are no established reports of human cases in which parabens have elicited an estrogen-mediated adverse event.^6,11

Concerns about a possible link between parabens and breast cancer have been largely diminished or relegated to the status of unknown and difficult to ascertain.¹³ Further, present knowledge provides no established link between the topical application of parabens-containing skin care formulations on healthy skin and cancer risk.¹⁰ Only intact skin should come in touch with products containing parabens to prevent irritant reactions.

Conclusion

Despite the fearful hype and reaction to one report 15 years ago, parabens continue to be safely used in numerous topical formulations. Their widespread use and lack of association with adverse events are a testament to their safety. There are no data to support discouraging patients from using parabens-containing products, which often are safer than other preservative alternatives. From a dermatologic perspective, this nonallergen of the year deserves a better reputation.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems. Write to her at dermnews@mdedge.com

References

1. “Goodman and Gilman’s The Pharmacological Basis of Therapeutics,” 6th ed. (New York: Macmillan, 1980, p. 969).

2. Toxicity: The Butyl, Ethyl, Methyl, and Propyl Esters have been found to promote allergic sensitization in humans, in “Dangerous Properties of Industrial Materials,” 4th ed. (New York: Van Nostrand Reinhold, 1975, p. 929).

3. Food Chem Toxicol. 2001 Jun;39(6):513-32.

4. Dermatitis. 2014 Sep-Oct;25(5):215-31.

5. Crit Rev Toxicol. 2005 Jun;35(5):435-58.

6. Int J Toxicol. 2008;27 Suppl 4:1-82.

7. Food Chem Toxicol. 2002 Oct;40(10):1335-73.

8. Dermatitis. 2019 Jan/Feb;30(1):3-31.

9. Exp Dermatol. 2007 Oct;16(10):830-6.

10. J Appl Toxicol. 2004 Jan-Feb;24(1):5-13.

11. Dermatitis. 2019 Jan/Feb;30(1):32-45.

12. Food Chem Toxicol. 2005 Feb;43(2):279-91.

13. Dermatitis. 2018 Dec 18. doi: 10.1097/DER.0000000000000429.

14. Dermatitis. 2018 Nov/Dec;29(6):297-309.

15. Food Chem Toxicol. 2005 Jul;43(7):985-1015.

 

Parabens were named nonallergen of the year! It is time that we help consumers understand that the substitutes for parabens are often worse than parabens, and parabens are not as sensitizing as we thought. Preservatives are essential parts of most cosmetics and cosmeceuticals. (I say “most” because many organic products do not have them and consequently have shorter shelf lives.) Without them, products are vulnerable to rapid decomposition and infiltration by bacteria, fungi, and molds. The preservatives that are used in the place of parabens often are sensitizers. What do we tell our patients about the safety of parabens with all of these conflicting reports? This column will focus on current thoughts regarding the safety of parabens used as preservatives. I would love to hear your thoughts.

Background

monticelllo/iStock/Getty Images Plus

Parabens are alkyl esters of p-hydroxybenzoic acid and have been used as a class of preservatives since the late 1920s and early 1930s. Parabens are found naturally in raspberries, blackberries, carrots, and cucumbers and are common ingredients in food and pharmaceuticals. They are still widely used in skin, hair, and body care products, despite the public outcry against them.^1-4

There are many kinds of parabens such as butylparaben, isobutylparaben, ethylparaben, methylparaben, propylparaben, isopropylparaben, and benzylparaben, each with its own characteristics.⁵ Parabens are considered ideal preservative ingredients because they exhibit a broad spectrum of antimicrobial activity, stability over a large pH and temperature range, have no odor, do not change color, and are water soluble enough to yield an effective concentration in a hydrophilic formulation.³ As the alkyl chain length of parabens increases, they become less water soluble and more oil soluble. Parabens penetrate the skin barrier in inverse relation to its ester chain length.⁶ Often, several parabens will be combined to take advantage of each paraben’s solubility characteristics.

Many patients avoid parabens because of “health risks.” Now other preservatives are being substituted for parabens, even though these ingredients may be less studied or even less safe than parabens. It is important not to lump all parabens together as they each have different characteristics. Methylparaben and propylparaben are the most commonly used parabens in skin care products.⁷ Combinations of parabens are notably more effective than the use of single parabens.^3,8 High concentrations of any type of paraben can cause an irritant reaction on the skin, but those with longer ester chain lengths are more likely to cause irritation.

Methylparaben

The methyl ester of p-hydroxybenzoic acid is found in many skin care products. It is readily absorbed through the skin and gastrointestinal tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body. Studies have shown it is nontoxic, nonirritating, and nonsensitizing. It is not teratogenic, embryotoxic, or carcinogenic. Methylparaben, because of its shorter side chain groups and greater lipophilicity, has been shown to be more readily absorbed by the skin than other paraben chemicals.^8,9 It is also on the low order of ingredients provoking acute and chronic toxicity.³

 

Propylparaben

Propylparaben is the ester form of p-hydroxybenzoic acid that has been esterified with n-propanol. It is the most commonly used antimicrobial preservative in foods, cosmetics, and drugs. It is readily absorbed through the skin and GI tract. It is quickly hydrolyzed and excreted in the urine and does not accumulate in the body.

Estrogenic activity of parabens

In a 2004 study, Darbre et al. reported on the discovery of parabens-like substances in breast tissue and published these findings in the Journal of Applied Toxicology.¹⁰ The media and public panicked, saying that parabens have estrogenic activity and can cause breast cancer. However, many studies have shown that certain parabens do not have estrogenic activity. Although some parabens have been shown to impart estrogenic effects in vitro, these are very weak. The four most commonly used parabens in cosmetic products are 10,000-fold or less potent than 17beta-estradiol.¹¹ The potential to result in an adverse effect mediated via an estrogen mode of action has not been established in humans.⁶ Paraben exposure differs geographically. No correlation has been found between the amount of parabens in a geographic location and the incidence of breast cancer. Current scientific knowledge is insufficient to demonstrate a clear cancer risk caused by the topical application of cosmetics that contain parabens on normal intact skin.¹¹

Parabens and contact dermatitis

Paraben compounds are capable of minimal penetrance through intact skin.¹² When they are able to penetrate the skin – a capacity that varies among the class – parabens are rapidly metabolized to p-hydroxybenzoic acid and promptly excreted in the urine.^3,11 Parabens for many years were thought to cause contact dermatitis, and there are many reports of this. However, the incidence is much lower than previously thought. In fact, parabens were named “Nonallergen of the Year in 2018” because of the low incidence of reactions in patch tests.¹³ Higher concentrations of parabens applied topically to skin – especially “nonintact” skin – have been shown to cause mild irritant reactions. It is likely that many of these reported cases of “contact dermatitis” were actually irritant dermatitis. Longstanding concerns about the allergenicity of parabens in relation to the skin have been rendered insignificant, as the wealth of evidence reveals little to no support for the cutaneous toxicity of these substances.¹¹ Yim et al. add that parabens remain far less sensitizing than agents newly introduced for use in personal care products.⁴

Daily average exposure to parabens

It is estimated that parabens are found in 10% of personal care products. In most cases, these products contain 1% or less of parabens. If the average patient uses 50 g of personal care products a day, then the average daily exposure to parabens topically is 0.05 g. Parabens also are found in food and drugs, so the total paraben exposure per day is assumed to be about 1 mg/day. (See the 2002 Food and Chemical Toxicology article for details of how this was calculated.)⁷ When food, personal care products, and drug exposure rates are added, the average person is exposed to 1.29 mg/kg per day or 77.5 mg/day for a 60-kg individual. You can see that personal care products account for a fraction of exposure, as most paraben exposure comes from food.

 

Government opinion on the safety of parabens for the skin

Parabens long have been assessed as safe for use in cosmetic products in many countries. The European Commission stipulated a maximum concentration of 0.4% for each paraben and 0.8% for total mixture of paraben esters.^4,6 While the Federal Food, Drug, and Cosmetic Act of 1938 prohibits the Food and Drug Administration from ruling on cosmetic ingredients, the industry-sponsored Cosmetic Ingredient Review expert panel has endorsed the European guidelines.^4,6 Further, the North American Contact Dermatitis Group has pointed out that parabens continue to demonstrate the lowest prevalence of positivity (0.6%) of any major preservative available on the North American market, which includes over 10,000 cosmetic and personal care products, and remain one of the safest classes of preservatives for the skin.¹⁴ Further, the FDA has listed or classified parabens as generally regarded as safe.⁸

Safety of parabens

Parabens do not accumulate in tissues or organs for any appreciable length of time.^6,8 In addition, carcinogenicity, cytotoxicity, or mutagenicity has not been proven in relation to parabens.⁸ Indeed, classical assays have shown no activity from parabens in terms of mutagenicity or carcinogenicity.^11,15 Some estrogenic effects or activity that mimics estrogen have been associated with parabens in vitro, but this activity has been noted as very weak and there are no established reports of human cases in which parabens have elicited an estrogen-mediated adverse event.^6,11

Concerns about a possible link between parabens and breast cancer have been largely diminished or relegated to the status of unknown and difficult to ascertain.¹³ Further, present knowledge provides no established link between the topical application of parabens-containing skin care formulations on healthy skin and cancer risk.¹⁰ Only intact skin should come in touch with products containing parabens to prevent irritant reactions.

Conclusion

Despite the fearful hype and reaction to one report 15 years ago, parabens continue to be safely used in numerous topical formulations. Their widespread use and lack of association with adverse events are a testament to their safety. There are no data to support discouraging patients from using parabens-containing products, which often are safer than other preservative alternatives. From a dermatologic perspective, this nonallergen of the year deserves a better reputation.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote two textbooks: “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and “Cosmeceuticals and Cosmetic Ingredients” (New York: McGraw-Hill, 2014), and a New York Times Best Sellers book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Evolus, Galderma, and Revance. She is the founder and CEO of Skin Type Solutions Franchise Systems. Write to her at dermnews@mdedge.com

References

1. “Goodman and Gilman’s The Pharmacological Basis of Therapeutics,” 6th ed. (New York: Macmillan, 1980, p. 969).

2. Toxicity: The Butyl, Ethyl, Methyl, and Propyl Esters have been found to promote allergic sensitization in humans, in “Dangerous Properties of Industrial Materials,” 4th ed. (New York: Van Nostrand Reinhold, 1975, p. 929).

3. Food Chem Toxicol. 2001 Jun;39(6):513-32.

4. Dermatitis. 2014 Sep-Oct;25(5):215-31.

5. Crit Rev Toxicol. 2005 Jun;35(5):435-58.

6. Int J Toxicol. 2008;27 Suppl 4:1-82.

7. Food Chem Toxicol. 2002 Oct;40(10):1335-73.

8. Dermatitis. 2019 Jan/Feb;30(1):3-31.

9. Exp Dermatol. 2007 Oct;16(10):830-6.

10. J Appl Toxicol. 2004 Jan-Feb;24(1):5-13.

11. Dermatitis. 2019 Jan/Feb;30(1):32-45.

12. Food Chem Toxicol. 2005 Feb;43(2):279-91.

13. Dermatitis. 2018 Dec 18. doi: 10.1097/DER.0000000000000429.

14. Dermatitis. 2018 Nov/Dec;29(6):297-309.

15. Food Chem Toxicol. 2005 Jul;43(7):985-1015.

 

Progressive macular hypomelanosis (PMH) presents as asymptomatic, ill-defined hypopigmented macules and patches on the trunk and back. They often coalesce near the midline, and occasionally extend beyond the trunk to the arms, legs, head, or neck. PMH is more frequently diagnosed among black individuals, although it affects all races and ethnicities. The natural history of PMH can vary from stable and progressive disease, and may resolve spontaneously after a few years. The pathogenesis of PMH remains unknown. It has been proposed that the hypopigmentation is caused by decreased melanin production and altered melanosome dispersal in reaction to Propionibacterium acnes.

PMH must be distinguished from some of its clinical mimickers, including vitiligo, hypopigmented mycosis fungoides, tinea versicolor, and pityriasis alba. Potassium hydroxide preparations can be performed in the office to evaluate for tinea versicolor. An additional tool to aid in diagnosis is the use of a Wood’s light. The lesions of PMH characteristically show punctiform orange-red follicular fluorescence when exposed to a Wood’s light, indicating the presence of a porphyrin-producing organism, presumably P. acnes. A skin biopsy is necessary to rule out hypopigmented mycosis fungoides.

Skin biopsy of PMH typically reveals decreased melanin with a normal number of melanocytes. In our patient, a punch biopsy of the right lateral arm demonstrated minimally decreased density of epidermal melanocytes with dermal pigment incontinence. SOX10 immunohistochemical staining demonstrated scattered melanocytes in the epidermis. Preserved melanin within keratinocytes was noted.

In our patient, there was significant spread to the face, which is highly unusual and has only been documented in a few case series. There are no standard recommendations for definitive treatment of PMH. Topical antimicrobial therapies, such as clindamycin solution and benzoyl peroxide gel, have been beneficial in some studies. Tetracyclines, narrow-band ultraviolet B phototherapy, and even isotretinoin have had some reported success.

This case and photo were submitted by Mr. Franzetti, Dr. Rush, and Dr. Shalin of the University of Arkansas for Medical Sciences, Little Rock.

Donna Bilu Martin, MD, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

 

Progressive macular hypomelanosis (PMH) presents as asymptomatic, ill-defined hypopigmented macules and patches on the trunk and back. They often coalesce near the midline, and occasionally extend beyond the trunk to the arms, legs, head, or neck. PMH is more frequently diagnosed among black individuals, although it affects all races and ethnicities. The natural history of PMH can vary from stable and progressive disease, and may resolve spontaneously after a few years. The pathogenesis of PMH remains unknown. It has been proposed that the hypopigmentation is caused by decreased melanin production and altered melanosome dispersal in reaction to Propionibacterium acnes.

PMH must be distinguished from some of its clinical mimickers, including vitiligo, hypopigmented mycosis fungoides, tinea versicolor, and pityriasis alba. Potassium hydroxide preparations can be performed in the office to evaluate for tinea versicolor. An additional tool to aid in diagnosis is the use of a Wood’s light. The lesions of PMH characteristically show punctiform orange-red follicular fluorescence when exposed to a Wood’s light, indicating the presence of a porphyrin-producing organism, presumably P. acnes. A skin biopsy is necessary to rule out hypopigmented mycosis fungoides.

Skin biopsy of PMH typically reveals decreased melanin with a normal number of melanocytes. In our patient, a punch biopsy of the right lateral arm demonstrated minimally decreased density of epidermal melanocytes with dermal pigment incontinence. SOX10 immunohistochemical staining demonstrated scattered melanocytes in the epidermis. Preserved melanin within keratinocytes was noted.

In our patient, there was significant spread to the face, which is highly unusual and has only been documented in a few case series. There are no standard recommendations for definitive treatment of PMH. Topical antimicrobial therapies, such as clindamycin solution and benzoyl peroxide gel, have been beneficial in some studies. Tetracyclines, narrow-band ultraviolet B phototherapy, and even isotretinoin have had some reported success.

This case and photo were submitted by Mr. Franzetti, Dr. Rush, and Dr. Shalin of the University of Arkansas for Medical Sciences, Little Rock.

Donna Bilu Martin, MD, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

 

Progressive macular hypomelanosis (PMH) presents as asymptomatic, ill-defined hypopigmented macules and patches on the trunk and back. They often coalesce near the midline, and occasionally extend beyond the trunk to the arms, legs, head, or neck. PMH is more frequently diagnosed among black individuals, although it affects all races and ethnicities. The natural history of PMH can vary from stable and progressive disease, and may resolve spontaneously after a few years. The pathogenesis of PMH remains unknown. It has been proposed that the hypopigmentation is caused by decreased melanin production and altered melanosome dispersal in reaction to Propionibacterium acnes.

PMH must be distinguished from some of its clinical mimickers, including vitiligo, hypopigmented mycosis fungoides, tinea versicolor, and pityriasis alba. Potassium hydroxide preparations can be performed in the office to evaluate for tinea versicolor. An additional tool to aid in diagnosis is the use of a Wood’s light. The lesions of PMH characteristically show punctiform orange-red follicular fluorescence when exposed to a Wood’s light, indicating the presence of a porphyrin-producing organism, presumably P. acnes. A skin biopsy is necessary to rule out hypopigmented mycosis fungoides.

Skin biopsy of PMH typically reveals decreased melanin with a normal number of melanocytes. In our patient, a punch biopsy of the right lateral arm demonstrated minimally decreased density of epidermal melanocytes with dermal pigment incontinence. SOX10 immunohistochemical staining demonstrated scattered melanocytes in the epidermis. Preserved melanin within keratinocytes was noted.

In our patient, there was significant spread to the face, which is highly unusual and has only been documented in a few case series. There are no standard recommendations for definitive treatment of PMH. Topical antimicrobial therapies, such as clindamycin solution and benzoyl peroxide gel, have been beneficial in some studies. Tetracyclines, narrow-band ultraviolet B phototherapy, and even isotretinoin have had some reported success.

This case and photo were submitted by Mr. Franzetti, Dr. Rush, and Dr. Shalin of the University of Arkansas for Medical Sciences, Little Rock.

Donna Bilu Martin, MD, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being. As the frequency of eating dinner with parents goes up, the rates of mood and anxiety disorders and high-risk behaviors in teenagers go down.

Wavebreakmedia/Thinkstock

But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.

Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.

 

Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.

Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.^1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.^3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.¹ Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.⁵

Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.⁶ And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.^7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.

It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.

 

Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.

Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.

While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.

Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.

At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

References

1. J Adolesc Health. 2006;39(3):337-45.

2. J Adolesc. 2010;33(1):187-96.

3. J Adolesc Health. 2009;44(5):431-6.

4. Health Psychol. 2008;27(Suppl 2):s109-17.

5. J Adolesc Health. 2009;45(4):389-95.

6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.

7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.

8. Prev Med. 2018;113:7-12.

Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being. As the frequency of eating dinner with parents goes up, the rates of mood and anxiety disorders and high-risk behaviors in teenagers go down.

Wavebreakmedia/Thinkstock

But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.

Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.

 

Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.

Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.^1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.^3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.¹ Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.⁵

Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.⁶ And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.^7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.

It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.

 

Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.

Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.

While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.

Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.

At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

References

1. J Adolesc Health. 2006;39(3):337-45.

2. J Adolesc. 2010;33(1):187-96.

3. J Adolesc Health. 2009;44(5):431-6.

4. Health Psychol. 2008;27(Suppl 2):s109-17.

5. J Adolesc Health. 2009;45(4):389-95.

6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.

7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.

8. Prev Med. 2018;113:7-12.

Intuitively, we have come to believe that adding more to each family members’ schedule – a lesson, an activity, more homework time – is more enriching or meaningful than is a family dinner, which appears to have less direct impact. However, there is a growing body of evidence that, when an entire family eats dinner together 5 or more nights weekly, the emotional health and well-being of all family members is improved. Not only is their health improved, as there is a greater likelihood of eating nutritious food, but so are a child’s school performance and emotional well-being. As the frequency of eating dinner with parents goes up, the rates of mood and anxiety disorders and high-risk behaviors in teenagers go down.

Wavebreakmedia/Thinkstock

But less than 60% of children eat five or more meals with their parents each week (National Center on Addiction and Substance Abuse [CASA], 2012). Few people would suggest that encouraging families to eat dinner together is a bad idea, but time is the ultimate scarce resource. Preparing food and eating together takes time, and parents and children have many demands on that time that feel nonnegotiable, such as homework, exercise, team practice, or work obligations. When you meet with your patients and explain the tremendous health benefits of eating dinner together, you help your patients and their parents make informed decisions about how to rebalance time to prioritize family dinners that have real but fewer obvious impacts then do a piano lesson or dance class.

Of course, children who eat regular family dinners eat more fruits and vegetables and fewer fried foods and soft drinks than do their peers who eat dinner with their families less often. They are less likely to become obese in youth and more likely to eat healthily and maintain a healthy weight once they live on their own as adults.

 

Scientific evidence of the mental health benefits to children of eating meals with their families first emerged in the 1990s when the National Center on Addiction and Substance Abuse at Columbia University, New York, began surveying various family behaviors and correlating them with the risk of adolescent substance use and misuse. They found strong evidence that when families ate dinner together five or more times weekly (we’ll call this “frequent family dinners”), their adolescents were far less likely to initiate alcohol and cigarette use and less likely to regularly abuse alcohol and drugs. Subsequent studies have demonstrated that the protective effect may be greater for girls than boys and may be greater for alcohol, cigarettes, and marijuana than for other drugs. But earlier age of first use of substances substantially raises the risk of later addiction, so the health benefits of any delay in first use are significant.

Since CASA’s first studies in the 1990s, researchers began paying closer attention to family meals and a variety of psychiatric problems in youth. They demonstrated that frequent family dinners lowered the risk of other externalizing behaviors in youth, including risky sexual behaviors, threats of physical harm, aggression, fights leading to injury, and carrying or using a weapon.^1,2 Frequent family dinners are associated with lower rates of disordered eating behaviors and disordered body image in adolescent girls.^3,4 Multiple studies have found a powerful association between frequent family dinners and lower rates of depressive symptoms and suicide attempts in both male and female adolescents.¹ Frequent family dinners even have been shown to mitigate against the risks of multiple poor health and academic outcomes in children with high adverse childhood experience (ACE) scores.⁵

Beyond protecting against problems, frequent family meals are associated with improved well-being and performance. Studies have demonstrated positive associations between frequent family meals and higher levels of self-esteem, self-efficacy, and well-being in adolescents, both male and female. They have consistently found significant associations between frequent family meals and higher grade point averages, commitment to learning, and rich vocabularies in children and adolescents, even after adjustment for demographic and other familial factors.⁶ And children are not the only ones who benefit. Frequent family meals even have been shown to be associated with higher self-reported levels of well-being and self-esteem, and lower levels of stress among parents.^7,8 While investing the time in preparing meals and eating them together may sound stressful, it’s clear the benefits outweigh the risks for parents as well as for their children.

It is important to set the framework for what really matters in a family dinner so that your patients can enjoy all of these benefits. Parents may assume that the meal must be prepared from scratch with only fresh, local, or organic ingredients. But what matters most is that the food is delicious and nutritious, and that the time spent eating (and preparing it) is fun, and promotes conversation and connection. Homemade food usually is more nutritious and will bring more of the physical health benefits, but many store-bought ingredients or even take-out options can be healthy and can promote time for the family to sit together and connect. If parents enjoy preparing food, then it’s worthwhile! And they should not worry about having every member of the family together at every meal. Even if only one parent and child are present for a dinner, they each will enjoy the benefits.

 

Parents can use this time to help promote good habits in their children. Talking about why manners matter while practicing them at the table is powerful for young children. Let them know manners are how we show people that we care about them, whether by taking turns talking or chewing with our mouths closed! Older children and adolescents can learn about how effort is an essential ingredient in every important area in life, from school to meals. Tell them that sometimes the work or effort will be uncomfortable, and pitching in to share the effort lightens everyone’s load. When parents ask for help, they show their children how to do the same and that they have confidence in their child’s ability to be helpful.

Parents should share the joy of the effort, too! They can invite their young children to help with the meal preparation in age-appropriate ways: pulling herbs off of their stems, rinsing vegetables, sprinkling spices, or emptying a box of spaghetti into a pot of water. Older children feel honored to be given bigger responsibilities, such as carrying plates to the table or cutting vegetables (with supervision, when appropriate). And adolescents, exploring their interests and enjoying their independence, may enjoy building their own menus for the family, doing the shopping or leading the preparation of a dish or full meal themselves.

While there is a role for supporting good manners and helpful habits, help parents avoid getting into power struggles with their children over what they will eat or how they conduct themselves at the table. There should be reasonable rules and expectations around mealtime, and predictable, reasonable consequences. If children try a food and don’t like it, they can have a bowl of (nutritious) cereal and stay at the table with the family. Phones should not be allowed at the table, and televisions should be off during the meal (although music may enhance the sense of pleasure or celebration). Mealtime should be time for relaxing, listening, and connecting.

Offer some ideas about how to facilitate conversations. Asking about how a child’s day went may spark conversations sometimes, but usually people benefit from specific questions. What made you really laugh today? What did you have for lunch? Whom did you sit next to on the bus? If a parent starts by telling a story about his or her day, even better! This is especially potent if a parent talks about something embarrassing or challenging, or mentions a failure. Young children will have plenty of these stories, and adolescents build resilience by internalizing the idea that setbacks and difficulties are a normal, healthy part of every day. This is a great time to talk about current events, whether in the news, entertainment, or sports. And telling stories about when children were younger, when the parents were children, or even about grandparents or more distant ancestors is a wonderful way to engage children in the greater story of their family narrative, and is always engaging and memorable.

At a deeper level, the family dinner is a time that recognizes each person’s contribution to a discussion, and facilitates a calm discussion of the families’ history and values. There is connection, communication, and building of trust. Families that cannot schedule a minimum number of dinners or that have dinners filled with tension and conflict, are very likely to have children at risk. For those conflicted and often unhappy families, a pediatrician’s early recognition and intervention could make a meaningful difference.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

References

1. J Adolesc Health. 2006;39(3):337-45.

2. J Adolesc. 2010;33(1):187-96.

3. J Adolesc Health. 2009;44(5):431-6.

4. Health Psychol. 2008;27(Suppl 2):s109-17.

5. J Adolesc Health. 2009;45(4):389-95.

6. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-945.

7. Arch Pediatr Adolesc Med. 2004;158(8):792-6.

8. Prev Med. 2018;113:7-12.

Long-acting injectables (LAIs) continue to be underused for patients with chronic diseases such as schizophrenia and bipolar disorder. However, in my practice, I have found the use of those medications to be useful for promoting adherence, and I wonder why they are not used more often – in light of their effectiveness. Specifically, among individuals with schizophrenia, LAIs can lead to significant improvements in symptom control, quality of life, and overall functioning.¹

The following three cases illustrate the power of LAIs:

Case 1: A male patient with schizoaffective diagnosis had been admitted several times to the inpatient psychiatric unit and had poor compliance to medications by mouth. He had multiple emergency department visits besides having community health behavioral support. After various medication trials by mouth, he responded to LAIs. He was able to function in the community for longer periods of time and required far fewer ED visits. He followed up with his outpatient psychiatric support regularly.

Case 2: A female patient with schizoaffective disorder had psychosis of a persecutory nature and paranoia. She was unable to function in the community and struggled with delusional thoughts leading to anger outbursts in the community. She continually refused medicines by mouth in the outpatient unit. Upon involuntary inpatient management as per court order, the patient responded to LAIs. Her insight improved, and she displayed better judgment in the future.

Case 3: A female patient with bipolar I was impulsive and promiscuous, and routinely entered into high-risk situations. She was not able to negotiate safely in the community, and was shuttling from shelter to shelter. She was losing her medications time and again during her transition in the community. She responded well to LAIs, however, and was able to keep herself out of the inpatient hospital for longer periods of time. She said she felt relieved about not depending on daily oral medications. She also reported not self medicating with street substances.

A recent retrospective study of more than 3,600 patients showed that those who initiate LAIs versus oral antipsychotics have greater reductions in the number of hospitalizations.² Furthermore, treatment with LAIs might be more cost-effective than oral medications, and might reduce the risk of suicide and the propensity to violence in at least a subset of individuals with psychotic illnesses and comorbid substance use disorders.^3,4

 

Introduction of LAI intervention within the treatment plan also might provide additional benefits and potentially reduce the burden on health care resources.⁵ Psychiatrists seem to use LAIs conservatively and tend to be too slow to introduce this intervention even after patients experience several acute episodes. Psychiatrists should inform patients about different forms of treatment, including LAIs, during the early stages of the illness.⁶

Improving medication adherence in physical and mental health care is of paramount importance for the effective care of patients. Psychiatrists and primary care physicians should be made aware of the anticipated benefits of this intervention.

References

1. Kaplan G et al. Impact of long-acting injectable antipsychotics on medication adherence and clinical, functional, and economic outcomes of schizophrenia. Patient Prefer Adherence. 2013;13:1171-80.

2. Brissos S et al. The role of long-acting injectable antipsychotics in schizophrenia: a critical appraisal. Therapeutic advances in psychopharmacology. 2014 Oct;4(5):198-219.

3. Ravasio R et al. Analisi di costo-efficacia dello switch da un antipsicotico orale a risperidone a rilascio prolungato nel trattamento dei pazienti affetti da schizofrenia. Giorn Ital Health Technol Ass. 2019;2:1-8.

4. Reichhart T and W Kissling. Societal costs of nonadherence in schizophrenia: homicide/suicide. Mind & Brain, J Psychiatry. 2010 Aug 1(2):29-32.

5. Offord S et al. Health care resource usage of schizophrenia patients initiating long-acting injectable antipsychotics vs oral. J Med Econ. 2013;16:231-9.

6. Matthias J and W Rossler. Attitudes toward long-acting depot antipsychotics: a survey of patients, relatives and psychiatrists. Psychiatry Res. 2010 Jan 30;175(1-2):58-62.

Dr. Lamba, a psychiatrist and medical director at BayRidge Hospital in Lynn, Mass., has no disclosures. He changed key facts about the patients discussed to protect their confidentiality.

Long-acting injectables (LAIs) continue to be underused for patients with chronic diseases such as schizophrenia and bipolar disorder. However, in my practice, I have found the use of those medications to be useful for promoting adherence, and I wonder why they are not used more often – in light of their effectiveness. Specifically, among individuals with schizophrenia, LAIs can lead to significant improvements in symptom control, quality of life, and overall functioning.¹

The following three cases illustrate the power of LAIs:

Case 1: A male patient with schizoaffective diagnosis had been admitted several times to the inpatient psychiatric unit and had poor compliance to medications by mouth. He had multiple emergency department visits besides having community health behavioral support. After various medication trials by mouth, he responded to LAIs. He was able to function in the community for longer periods of time and required far fewer ED visits. He followed up with his outpatient psychiatric support regularly.

Case 2: A female patient with schizoaffective disorder had psychosis of a persecutory nature and paranoia. She was unable to function in the community and struggled with delusional thoughts leading to anger outbursts in the community. She continually refused medicines by mouth in the outpatient unit. Upon involuntary inpatient management as per court order, the patient responded to LAIs. Her insight improved, and she displayed better judgment in the future.

Case 3: A female patient with bipolar I was impulsive and promiscuous, and routinely entered into high-risk situations. She was not able to negotiate safely in the community, and was shuttling from shelter to shelter. She was losing her medications time and again during her transition in the community. She responded well to LAIs, however, and was able to keep herself out of the inpatient hospital for longer periods of time. She said she felt relieved about not depending on daily oral medications. She also reported not self medicating with street substances.

A recent retrospective study of more than 3,600 patients showed that those who initiate LAIs versus oral antipsychotics have greater reductions in the number of hospitalizations.² Furthermore, treatment with LAIs might be more cost-effective than oral medications, and might reduce the risk of suicide and the propensity to violence in at least a subset of individuals with psychotic illnesses and comorbid substance use disorders.^3,4

 

Introduction of LAI intervention within the treatment plan also might provide additional benefits and potentially reduce the burden on health care resources.⁵ Psychiatrists seem to use LAIs conservatively and tend to be too slow to introduce this intervention even after patients experience several acute episodes. Psychiatrists should inform patients about different forms of treatment, including LAIs, during the early stages of the illness.⁶

Improving medication adherence in physical and mental health care is of paramount importance for the effective care of patients. Psychiatrists and primary care physicians should be made aware of the anticipated benefits of this intervention.

References

1. Kaplan G et al. Impact of long-acting injectable antipsychotics on medication adherence and clinical, functional, and economic outcomes of schizophrenia. Patient Prefer Adherence. 2013;13:1171-80.

2. Brissos S et al. The role of long-acting injectable antipsychotics in schizophrenia: a critical appraisal. Therapeutic advances in psychopharmacology. 2014 Oct;4(5):198-219.

3. Ravasio R et al. Analisi di costo-efficacia dello switch da un antipsicotico orale a risperidone a rilascio prolungato nel trattamento dei pazienti affetti da schizofrenia. Giorn Ital Health Technol Ass. 2019;2:1-8.

4. Reichhart T and W Kissling. Societal costs of nonadherence in schizophrenia: homicide/suicide. Mind & Brain, J Psychiatry. 2010 Aug 1(2):29-32.

5. Offord S et al. Health care resource usage of schizophrenia patients initiating long-acting injectable antipsychotics vs oral. J Med Econ. 2013;16:231-9.

6. Matthias J and W Rossler. Attitudes toward long-acting depot antipsychotics: a survey of patients, relatives and psychiatrists. Psychiatry Res. 2010 Jan 30;175(1-2):58-62.

Dr. Lamba, a psychiatrist and medical director at BayRidge Hospital in Lynn, Mass., has no disclosures. He changed key facts about the patients discussed to protect their confidentiality.

Long-acting injectables (LAIs) continue to be underused for patients with chronic diseases such as schizophrenia and bipolar disorder. However, in my practice, I have found the use of those medications to be useful for promoting adherence, and I wonder why they are not used more often – in light of their effectiveness. Specifically, among individuals with schizophrenia, LAIs can lead to significant improvements in symptom control, quality of life, and overall functioning.¹

The following three cases illustrate the power of LAIs:

Case 1: A male patient with schizoaffective diagnosis had been admitted several times to the inpatient psychiatric unit and had poor compliance to medications by mouth. He had multiple emergency department visits besides having community health behavioral support. After various medication trials by mouth, he responded to LAIs. He was able to function in the community for longer periods of time and required far fewer ED visits. He followed up with his outpatient psychiatric support regularly.

Case 2: A female patient with schizoaffective disorder had psychosis of a persecutory nature and paranoia. She was unable to function in the community and struggled with delusional thoughts leading to anger outbursts in the community. She continually refused medicines by mouth in the outpatient unit. Upon involuntary inpatient management as per court order, the patient responded to LAIs. Her insight improved, and she displayed better judgment in the future.

Case 3: A female patient with bipolar I was impulsive and promiscuous, and routinely entered into high-risk situations. She was not able to negotiate safely in the community, and was shuttling from shelter to shelter. She was losing her medications time and again during her transition in the community. She responded well to LAIs, however, and was able to keep herself out of the inpatient hospital for longer periods of time. She said she felt relieved about not depending on daily oral medications. She also reported not self medicating with street substances.

A recent retrospective study of more than 3,600 patients showed that those who initiate LAIs versus oral antipsychotics have greater reductions in the number of hospitalizations.² Furthermore, treatment with LAIs might be more cost-effective than oral medications, and might reduce the risk of suicide and the propensity to violence in at least a subset of individuals with psychotic illnesses and comorbid substance use disorders.^3,4

 

Introduction of LAI intervention within the treatment plan also might provide additional benefits and potentially reduce the burden on health care resources.⁵ Psychiatrists seem to use LAIs conservatively and tend to be too slow to introduce this intervention even after patients experience several acute episodes. Psychiatrists should inform patients about different forms of treatment, including LAIs, during the early stages of the illness.⁶

Improving medication adherence in physical and mental health care is of paramount importance for the effective care of patients. Psychiatrists and primary care physicians should be made aware of the anticipated benefits of this intervention.

References

1. Kaplan G et al. Impact of long-acting injectable antipsychotics on medication adherence and clinical, functional, and economic outcomes of schizophrenia. Patient Prefer Adherence. 2013;13:1171-80.

2. Brissos S et al. The role of long-acting injectable antipsychotics in schizophrenia: a critical appraisal. Therapeutic advances in psychopharmacology. 2014 Oct;4(5):198-219.

3. Ravasio R et al. Analisi di costo-efficacia dello switch da un antipsicotico orale a risperidone a rilascio prolungato nel trattamento dei pazienti affetti da schizofrenia. Giorn Ital Health Technol Ass. 2019;2:1-8.

4. Reichhart T and W Kissling. Societal costs of nonadherence in schizophrenia: homicide/suicide. Mind & Brain, J Psychiatry. 2010 Aug 1(2):29-32.

5. Offord S et al. Health care resource usage of schizophrenia patients initiating long-acting injectable antipsychotics vs oral. J Med Econ. 2013;16:231-9.

6. Matthias J and W Rossler. Attitudes toward long-acting depot antipsychotics: a survey of patients, relatives and psychiatrists. Psychiatry Res. 2010 Jan 30;175(1-2):58-62.

Dr. Lamba, a psychiatrist and medical director at BayRidge Hospital in Lynn, Mass., has no disclosures. He changed key facts about the patients discussed to protect their confidentiality.