Pediatrics

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

To the Editor:

Hemorrhagic lacrimation and epistaxis are dramatic presentations with a narrow differential diagnosis. It rarely has been reported to present alongside the more typical features of acute hemorrhagic edema of infancy (AHEI), which is a benign self-limited leukocytoclastic vasculitis most often seen in children aged 4 months to 2 years. Extracutaneous involvement rarely is seen in AHEI, though joint, gastrointestinal tract, and renal involvement have been reported.¹ Most patients present with edematous, annular, or cockade purpuric vasculitic lesions classically involving the face and distal extremities with relative sparing of the trunk. We present a case of a well-appearing, 10-month-old infant boy with hemorrhagic vasculitic lesions, acral edema, and an associated episode of hemorrhagic lacrimation and epistaxis.

A 10-month-old infant boy who was otherwise healthy presented to the emergency department (ED) with an acute-onset, progressively worsening cutaneous eruption of 2 days’ duration. A thorough history revealed that the eruption initially had presented as several small, bright-red papules on the thighs. The eruption subsequently spread to involve the buttocks, legs, and arms (Figures 1 and 2). The parents also noted that the patient had experienced an episode of bloody tears and epistaxis that lasted a few minutes at the pediatrician’s office earlier that morning, a finding that prompted the urgent referral to the ED.

Dermatology was then consulted. A review of systems was notable for rhinorrhea and diarrhea during the week leading to the eruption. The patient’s parents denied fevers, decreased oral intake, or a recent course of antibiotics. The patient’s medical history was notable only for atopic dermatitis treated with emollients and occasional topical steroids. The parents denied recent travel or vaccinations. Physical examination showed an afebrile, well-appearing infant with multiple nontender, slightly edematous, circular, purpuric papules and plaques scattered on the buttocks and extremities with edema on the dorsal feet. The remainder of the patient’s workup in the ED was notable for mild elevations in C-reactive protein levels (1.4 mg/dL [reference range, 0–1.2 mg/dL]) and an elevated erythrocyte sedimentation rate (22 mm/h [reference range, 2–12 mm/h]). A complete blood cell count; liver function tests; urinalysis; and coagulation studies, including prothrombin, partial thromboplastin time, and international normalized ratio, were unremarkable. Acute hemorrhagic edema of infancy was diagnosed based on the clinical manifestations.

Acute hemorrhagic edema of infancy (also known as Finkelstein disease, medallionlike purpura, Seidemayer syndrome, infantile postinfectious irislike purpura and edema, and purpura en cocarde avec oedeme) is believed to result from an immune complex–related reaction, often in the setting of an upper respiratory tract infection; medications, especially antibiotics; or vaccinations. The condition previously was considered a benign form of Henoch-Schönlein purpura; however, it is now recognized as its own clinical entity. Acute hemorrhagic edema of infancy commonly affects children between the ages of 4 months and 2 years. The incidence peaks in the winter months, and males tend to be more affected than females.¹

Acute hemorrhagic edema of infancy is clinically characterized by a triad of large purpuric lesions, low-grade fever, and peripheral acral edema. Edema can develop on the hands, feet, and genitalia. Importantly, facial edema has been noted to precede skin lesions.² Coin-shaped or targetoid hemorrhagic and purpuric lesions in a cockade or rosette pattern with scalloped margins typically begin on the distal extremities and tend to spread proximally. The lesions are variable in size but have been reported to be as large as 5 cm in diameter. Although joint pain, bloody diarrhea, hematuria, and proteinuria can accompany AHEI, most cases are devoid of systemic symptoms.³ Hemorrhagic lacrimation and epistaxis—both present in our patient—are rare findings with AHEI. It is likely that most providers, including dermatologists, may be unfamiliar with these striking clinical findings. Although the pathophysiology of hemorrhagic lacrimation and epistaxis has not been formally investigated, we postulate that it likely is related to the formation of immune complexes that lead to small vessel vasculitis, underpinning the characteristic findings in AHEI.^4,5 This reasoning is supported by the complete resolution of symptoms corresponding with clinical clearance of the cutaneous vasculitis in 2 prior cases^4,5 as well as in our patient who did not have a relapse of symptoms following cessation of the cutaneous eruption at a pediatric follow-up appointment 2 weeks later.

Acute hemorrhagic edema of infancy is a clinical diagnosis; however, a skin biopsy can be performed to confirm the clinical suspicion and rule out more serious conditions. Histopathologic examination reveals a leukocytoclastic vasculitis involving the capillaries and postcapillary venules of the upper and mid dermis. Laboratory test results usually are nonspecific but can help distinguish AHEI from more serious diseases. The erythrocyte sedimentation rate and C-reactive protein level may be slightly elevated in infants with AHEI. Urinalysis and stool guaiac tests also can be performed to evaluate for any renal or gastrointestinal involvement.⁶

The differential diagnosis includes IgA vasculitis, erythema multiforme, acute meningococcemia, urticarial vasculitis, Kawasaki disease, and child abuse. IgA vasculitis often presents with more systemic involvement, with abdominal pain, vomiting, hematemesis, diarrhea, and hematochezia occurring in up to 50% of patients. The cutaneous findings of erythema multiforme classically are confined to the limbs and face, and edema of the extremities typically is not seen. Patients with acute meningococcemia appear toxic with high fevers, malaise, and possible septic shock.⁵

Acute hemorrhagic edema of infancy is a self-limited condition typically lasting 1 to 3 weeks and requires only supportive care.⁷ Antibiotics should be given to treat concurrent bacterial infections, and antihistamines and steroids may be useful for symptomatic relief. Importantly, however, systemic corticosteroids do not appear to conclusively alter the disease course.⁸

Acute hemorrhagic edema of infancy is a rare benign leukocytoclastic vasculitis with a striking presentation often seen following an upper respiratory tract infection or course of antibiotics. Our case demonstrates that on rare occasions, AHEI may be accompanied by hemorrhagic lacrimation and epistaxis—findings that can be quite alarming to both parents and medical providers. Nonetheless, patients and their caretakers should be assured that the condition is self-limited and resolves without permanent sequalae.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Although new COVID-19 cases in children, as measured by the American Academy of Pediatrics and the Children’s Hospital Association, have remained fairly steady in recent months, data from the Centers for Diseases Control and Prevention suggest that weekly cases took a big jump in early January.

For the most recent week covered in the AAP/CHA weekly report, Jan. 20-26, there were over 36,000 child COVID cases reported in the United States, an increase of 8.8% from the week before (Jan. 13-19). New cases for the first 2 weeks of the year – 31,000 for the week of Dec. 30 to Jan. 5 and 26,000 during Jan. 6-12 – were consistent with the AAP/CHA assertion that “weekly reported child cases have plateaued at an average of about 32,000 cases ... over the past 4 months.”

The CDC data, however, show that new cases doubled during the week of Jan. 1-7 to over 65,000, compared with the end of December, and stayed at that level for Jan. 8-14, and since CDC figures are subject to a 6-week reporting delay, the final numbers are likely to be even higher. The composition by age changed somewhat between the 2 weeks, though, as those aged 0-4 years went from almost half of all cases in the first week down to 40% in the second, while cases rose for children aged 5-11 and 12-15, based on data from the COVID-19 response team.

Emergency department visits for January do not show a corresponding increase. ED visits among children aged 0-11 years with COVID-19, measured as a percentage of all ED visits, declined over the course of the month, as did visits for 16- and 17-year-olds, while those aged 12-15 started the month at 1.4% and were at 1.4% on Jan. 27, with a slight dip down to 1.2% in between, the CDC said on its COVID Data Tracker. Daily hospitalizations for children aged 0-17 also declined through mid-January and did not reflect the jump in new cases.

Meanwhile, vaccinated children are still in the minority: 57% of those under age 18 have received no COVID vaccine yet, the AAP said in a separate report. Just 7.4% of children under age 2 years had received at least one dose as of Jan. 25, as had 10.1% of those aged 2-4 years, 39.6% of 5- to 11-year-olds and 71.8% of those 12-17 years old, according to the CDC, with corresponding figures for completion of the primary series at 3.5%, 5.3%, 32.5%, and 61.5%.

Although new COVID-19 cases in children, as measured by the American Academy of Pediatrics and the Children’s Hospital Association, have remained fairly steady in recent months, data from the Centers for Diseases Control and Prevention suggest that weekly cases took a big jump in early January.

For the most recent week covered in the AAP/CHA weekly report, Jan. 20-26, there were over 36,000 child COVID cases reported in the United States, an increase of 8.8% from the week before (Jan. 13-19). New cases for the first 2 weeks of the year – 31,000 for the week of Dec. 30 to Jan. 5 and 26,000 during Jan. 6-12 – were consistent with the AAP/CHA assertion that “weekly reported child cases have plateaued at an average of about 32,000 cases ... over the past 4 months.”

The CDC data, however, show that new cases doubled during the week of Jan. 1-7 to over 65,000, compared with the end of December, and stayed at that level for Jan. 8-14, and since CDC figures are subject to a 6-week reporting delay, the final numbers are likely to be even higher. The composition by age changed somewhat between the 2 weeks, though, as those aged 0-4 years went from almost half of all cases in the first week down to 40% in the second, while cases rose for children aged 5-11 and 12-15, based on data from the COVID-19 response team.

Emergency department visits for January do not show a corresponding increase. ED visits among children aged 0-11 years with COVID-19, measured as a percentage of all ED visits, declined over the course of the month, as did visits for 16- and 17-year-olds, while those aged 12-15 started the month at 1.4% and were at 1.4% on Jan. 27, with a slight dip down to 1.2% in between, the CDC said on its COVID Data Tracker. Daily hospitalizations for children aged 0-17 also declined through mid-January and did not reflect the jump in new cases.

Meanwhile, vaccinated children are still in the minority: 57% of those under age 18 have received no COVID vaccine yet, the AAP said in a separate report. Just 7.4% of children under age 2 years had received at least one dose as of Jan. 25, as had 10.1% of those aged 2-4 years, 39.6% of 5- to 11-year-olds and 71.8% of those 12-17 years old, according to the CDC, with corresponding figures for completion of the primary series at 3.5%, 5.3%, 32.5%, and 61.5%.

Although new COVID-19 cases in children, as measured by the American Academy of Pediatrics and the Children’s Hospital Association, have remained fairly steady in recent months, data from the Centers for Diseases Control and Prevention suggest that weekly cases took a big jump in early January.

For the most recent week covered in the AAP/CHA weekly report, Jan. 20-26, there were over 36,000 child COVID cases reported in the United States, an increase of 8.8% from the week before (Jan. 13-19). New cases for the first 2 weeks of the year – 31,000 for the week of Dec. 30 to Jan. 5 and 26,000 during Jan. 6-12 – were consistent with the AAP/CHA assertion that “weekly reported child cases have plateaued at an average of about 32,000 cases ... over the past 4 months.”

The CDC data, however, show that new cases doubled during the week of Jan. 1-7 to over 65,000, compared with the end of December, and stayed at that level for Jan. 8-14, and since CDC figures are subject to a 6-week reporting delay, the final numbers are likely to be even higher. The composition by age changed somewhat between the 2 weeks, though, as those aged 0-4 years went from almost half of all cases in the first week down to 40% in the second, while cases rose for children aged 5-11 and 12-15, based on data from the COVID-19 response team.

Emergency department visits for January do not show a corresponding increase. ED visits among children aged 0-11 years with COVID-19, measured as a percentage of all ED visits, declined over the course of the month, as did visits for 16- and 17-year-olds, while those aged 12-15 started the month at 1.4% and were at 1.4% on Jan. 27, with a slight dip down to 1.2% in between, the CDC said on its COVID Data Tracker. Daily hospitalizations for children aged 0-17 also declined through mid-January and did not reflect the jump in new cases.

Meanwhile, vaccinated children are still in the minority: 57% of those under age 18 have received no COVID vaccine yet, the AAP said in a separate report. Just 7.4% of children under age 2 years had received at least one dose as of Jan. 25, as had 10.1% of those aged 2-4 years, 39.6% of 5- to 11-year-olds and 71.8% of those 12-17 years old, according to the CDC, with corresponding figures for completion of the primary series at 3.5%, 5.3%, 32.5%, and 61.5%.

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

A version of this article first appeared on Medscape.com.

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

A version of this article first appeared on Medscape.com.

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

A version of this article first appeared on Medscape.com.

The U.S. Surgeon General says 13 years old is too young to begin using social media.

Most social media platforms including TikTok, Snapchat, Instagram, and Facebook allow users to create accounts if they say they are at least 13 years old.

“I, personally, based on the data I’ve seen, believe that 13 is too early. ... It’s a time where it’s really important for us to be thoughtful about what’s going into how they think about their own self-worth and their relationships, and the skewed and often distorted environment of social media often does a disservice to many of those children,” U.S. Surgeon General Vivek Murthy, MD, told CNN.

Research has shown that teens are susceptible to cyberbullying and serious mental health impacts from social media usage and online activity during an era when the influence of the Internet has become everywhere for young people.

According to the Pew Research Center, 95% of teens age 13 and up have a smartphone, and 97% of teens say they use the Internet daily. Among 13- and 14-year-olds, 61% say they use TikTok and 51% say they use Snapchat. Older teens ages 15-17 use those social media platforms at higher rates, with 71% saying they use TikTok and 65% using Snapchat.

“If parents can band together and say you know, as a group, we’re not going to allow our kids to use social media until 16 or 17 or 18 or whatever age they choose, that’s a much more effective strategy in making sure your kids don’t get exposed to harm early,” Dr. Murthy said.

A version of this article originally appeared on WebMD.com.

The U.S. Surgeon General says 13 years old is too young to begin using social media.

Most social media platforms including TikTok, Snapchat, Instagram, and Facebook allow users to create accounts if they say they are at least 13 years old.

“I, personally, based on the data I’ve seen, believe that 13 is too early. ... It’s a time where it’s really important for us to be thoughtful about what’s going into how they think about their own self-worth and their relationships, and the skewed and often distorted environment of social media often does a disservice to many of those children,” U.S. Surgeon General Vivek Murthy, MD, told CNN.

Research has shown that teens are susceptible to cyberbullying and serious mental health impacts from social media usage and online activity during an era when the influence of the Internet has become everywhere for young people.

According to the Pew Research Center, 95% of teens age 13 and up have a smartphone, and 97% of teens say they use the Internet daily. Among 13- and 14-year-olds, 61% say they use TikTok and 51% say they use Snapchat. Older teens ages 15-17 use those social media platforms at higher rates, with 71% saying they use TikTok and 65% using Snapchat.

“If parents can band together and say you know, as a group, we’re not going to allow our kids to use social media until 16 or 17 or 18 or whatever age they choose, that’s a much more effective strategy in making sure your kids don’t get exposed to harm early,” Dr. Murthy said.

A version of this article originally appeared on WebMD.com.

The U.S. Surgeon General says 13 years old is too young to begin using social media.

Most social media platforms including TikTok, Snapchat, Instagram, and Facebook allow users to create accounts if they say they are at least 13 years old.

“I, personally, based on the data I’ve seen, believe that 13 is too early. ... It’s a time where it’s really important for us to be thoughtful about what’s going into how they think about their own self-worth and their relationships, and the skewed and often distorted environment of social media often does a disservice to many of those children,” U.S. Surgeon General Vivek Murthy, MD, told CNN.

Research has shown that teens are susceptible to cyberbullying and serious mental health impacts from social media usage and online activity during an era when the influence of the Internet has become everywhere for young people.

According to the Pew Research Center, 95% of teens age 13 and up have a smartphone, and 97% of teens say they use the Internet daily. Among 13- and 14-year-olds, 61% say they use TikTok and 51% say they use Snapchat. Older teens ages 15-17 use those social media platforms at higher rates, with 71% saying they use TikTok and 65% using Snapchat.

“If parents can band together and say you know, as a group, we’re not going to allow our kids to use social media until 16 or 17 or 18 or whatever age they choose, that’s a much more effective strategy in making sure your kids don’t get exposed to harm early,” Dr. Murthy said.

A version of this article originally appeared on WebMD.com.

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.

The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.

The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp. 

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

The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.

Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.^1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.¹ Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.² Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.^1,2 

Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.³

Differential includes congenital hemangiomas, pyogenic granulomas

Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:

Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.⁴

Continue to: Pyogenic granulomas

Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.

Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.⁵ Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.⁵

Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.⁴ Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.⁴ 

Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.⁵ Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.⁵ 

Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.⁵ 

Continue to: Individualize treatment when it's needed

Individualize treatment when it’s needed

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.² That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.⁶ Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.

Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.⁶ Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.² This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.

Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was ­tolerated, this was increased to 2 mg/kg/d ­for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.

After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.

A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.

The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.

The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp. 

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

The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.

Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.^1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.¹ Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.² Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.^1,2 

Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.³

Differential includes congenital hemangiomas, pyogenic granulomas

Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:

Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.⁴

Continue to: Pyogenic granulomas

Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.

Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.⁵ Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.⁵

Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.⁴ Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.⁴ 

Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.⁵ Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.⁵ 

Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.⁵ 

Continue to: Individualize treatment when it's needed

Individualize treatment when it’s needed

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.² That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.⁶ Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.

Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.⁶ Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.² This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.

Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was ­tolerated, this was increased to 2 mg/kg/d ­for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.

After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.

A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.

The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.

The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp. 

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

The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.

Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.^1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.¹ Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.² Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.^1,2 

Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.³

Differential includes congenital hemangiomas, pyogenic granulomas

Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:

Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.⁴

Continue to: Pyogenic granulomas

Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.

Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.⁵ Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.⁵

Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.⁴ Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.⁴ 

Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.⁵ Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.⁵ 

Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.⁵ 

Continue to: Individualize treatment when it's needed

Individualize treatment when it’s needed

The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.² That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.⁶ Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.

Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.⁶ Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.² This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.

Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was ­tolerated, this was increased to 2 mg/kg/d ­for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.

After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

A version of this article first appeared on Medscape.com.

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

A version of this article first appeared on Medscape.com.

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

A version of this article first appeared on Medscape.com.

THE CASE

James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.

Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.

James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.

The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.

● How would you proceed with this patient?

* The patient’s name has been changed to protect his identity.

James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.^1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.³ Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.

ADHD features can vary by age and sex

ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.⁴ Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).⁴

Psychostimulants are preferred for ADHD. However, a variety of medications are available and may prove efficacious as children grow and their symptoms and the capacity to manage them change.

The rate of heritability is high, with significant incidence among first-degree relatives.⁴ Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).^4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.^1,6 It persists among 2.6% to 6.8% of adults worldwide.⁷

Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).^1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.¹

The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.

Continue to: Begin with a screening tool, move to a clinical interview

When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.^5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.⁹

Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.¹⁰ However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,⁴ the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.⁶ Standardized meas­ures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 2^10-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.

Consider comorbidities and alternate diagnoses

The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.^4,6 In a 2016 study, approximately 64% of children with ADHD exhibited another developmental or psychiatric disorder at some point. These disorders included oppositional defiant or conduct disorders (52%), anxiety (33%), depression (17%), and autism spectrum disorder (14%), as well as Tourette syndrome, learning or language disorders, motor delays, substance use disorders, sleep-wake disorders, personality disorders, and ­suicidality.¹⁸

Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.^6,19Although further research is needed to ascertain potential associations between recurrent otitis media and language delay and later social, cognitive, or attention challenges, early consultation with an otolaryngologist is warranted if such concerns arise in a child’s early years.²⁰ Following the initial assessment, conduct a targeted examination and lab testing to rule out co-occurring conditions or comorbidities.

If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.²¹

Continue to: Risks that arise over time

Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).^4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.^4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.³ Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.

Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.⁶

A guide to pharmacotherapy

Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.² Treatment for ADHD can include behavioral therapy and medication.² AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on ­caregiver-, teacher-, or clinician-­administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line ­treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).⁶

Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and ­adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.

More than twothirds of ADHD patients with a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.

Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.⁶ Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.

Continue to: Once medication is stabilized...

Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.^5,6,22

Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.²² Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).²²

Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.^6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.

How multilevel care coordination can work

As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-­education and mindfulness-based stress reduction training for caregivers^24,25; occupational,²⁶ cognitive behavioral,²⁷ or family therapies^28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.^5,8

Evidence shows that recognition and diagnostic specificity of ADHD and comorbidities— not true prevalence—vary more widely among minority than among nonminority populations.

Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.²³ Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).

Continue to: Assess patients' needs and the resources available

Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.³⁰ Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.

Steps to ensuring health care equity

Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.³¹ In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,³² contributing to the 23% of children with ADHD who receive no treatment at all.²

Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.^2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.³¹ In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.

Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.

Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.⁴ Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.³³

Continue to: Impact of the COVID-19 pandemic

Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.^34,35

However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)

THE CASE

During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.

The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).

The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and ­parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.

After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed ­extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.

By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.

CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; [email protected]

THE CASE

James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.

Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.

James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.

The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.

● How would you proceed with this patient?

* The patient’s name has been changed to protect his identity.

James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.^1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.³ Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.

ADHD features can vary by age and sex

ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.⁴ Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).⁴

Psychostimulants are preferred for ADHD. However, a variety of medications are available and may prove efficacious as children grow and their symptoms and the capacity to manage them change.

The rate of heritability is high, with significant incidence among first-degree relatives.⁴ Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).^4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.^1,6 It persists among 2.6% to 6.8% of adults worldwide.⁷

Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).^1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.¹

The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.

Continue to: Begin with a screening tool, move to a clinical interview

When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.^5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.⁹

Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.¹⁰ However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,⁴ the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.⁶ Standardized meas­ures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 2^10-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.

Consider comorbidities and alternate diagnoses

The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.^4,6 In a 2016 study, approximately 64% of children with ADHD exhibited another developmental or psychiatric disorder at some point. These disorders included oppositional defiant or conduct disorders (52%), anxiety (33%), depression (17%), and autism spectrum disorder (14%), as well as Tourette syndrome, learning or language disorders, motor delays, substance use disorders, sleep-wake disorders, personality disorders, and ­suicidality.¹⁸

Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.^6,19Although further research is needed to ascertain potential associations between recurrent otitis media and language delay and later social, cognitive, or attention challenges, early consultation with an otolaryngologist is warranted if such concerns arise in a child’s early years.²⁰ Following the initial assessment, conduct a targeted examination and lab testing to rule out co-occurring conditions or comorbidities.

If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.²¹

Continue to: Risks that arise over time

Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).^4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.^4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.³ Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.

Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.⁶

A guide to pharmacotherapy

Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.² Treatment for ADHD can include behavioral therapy and medication.² AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on ­caregiver-, teacher-, or clinician-­administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line ­treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).⁶

Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and ­adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.

More than twothirds of ADHD patients with a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.

Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.⁶ Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.

Continue to: Once medication is stabilized...

Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.^5,6,22

Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.²² Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).²²

Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.^6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.

How multilevel care coordination can work

As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-­education and mindfulness-based stress reduction training for caregivers^24,25; occupational,²⁶ cognitive behavioral,²⁷ or family therapies^28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.^5,8

Evidence shows that recognition and diagnostic specificity of ADHD and comorbidities— not true prevalence—vary more widely among minority than among nonminority populations.

Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.²³ Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).

Continue to: Assess patients' needs and the resources available

Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.³⁰ Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.

Steps to ensuring health care equity

Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.³¹ In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,³² contributing to the 23% of children with ADHD who receive no treatment at all.²

Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.^2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.³¹ In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.

Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.

Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.⁴ Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.³³

Continue to: Impact of the COVID-19 pandemic

Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.^34,35

However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)

THE CASE

During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.

The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).

The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and ­parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.

After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed ­extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.

By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.

CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; [email protected]

THE CASE

James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.

Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.

James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.

The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.

● How would you proceed with this patient?

* The patient’s name has been changed to protect his identity.

James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.^1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.³ Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.

ADHD features can vary by age and sex

ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.⁴ Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).⁴

Psychostimulants are preferred for ADHD. However, a variety of medications are available and may prove efficacious as children grow and their symptoms and the capacity to manage them change.

The rate of heritability is high, with significant incidence among first-degree relatives.⁴ Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).^4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.^1,6 It persists among 2.6% to 6.8% of adults worldwide.⁷

Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).^1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.¹

The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.

Continue to: Begin with a screening tool, move to a clinical interview

When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.^5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.⁹

Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.¹⁰ However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,⁴ the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.⁶ Standardized meas­ures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 2^10-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.

Consider comorbidities and alternate diagnoses

The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.^4,6 In a 2016 study, approximately 64% of children with ADHD exhibited another developmental or psychiatric disorder at some point. These disorders included oppositional defiant or conduct disorders (52%), anxiety (33%), depression (17%), and autism spectrum disorder (14%), as well as Tourette syndrome, learning or language disorders, motor delays, substance use disorders, sleep-wake disorders, personality disorders, and ­suicidality.¹⁸

Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.^6,19Although further research is needed to ascertain potential associations between recurrent otitis media and language delay and later social, cognitive, or attention challenges, early consultation with an otolaryngologist is warranted if such concerns arise in a child’s early years.²⁰ Following the initial assessment, conduct a targeted examination and lab testing to rule out co-occurring conditions or comorbidities.

If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.²¹

Continue to: Risks that arise over time

Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).^4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.^4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.³ Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.

Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.⁶

A guide to pharmacotherapy

Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.² Treatment for ADHD can include behavioral therapy and medication.² AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on ­caregiver-, teacher-, or clinician-­administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line ­treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).⁶

Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and ­adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.

More than twothirds of ADHD patients with a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.

Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.⁶ Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.

Continue to: Once medication is stabilized...

Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.^5,6,22

Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.²² Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).²²

Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.^6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.

How multilevel care coordination can work

As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-­education and mindfulness-based stress reduction training for caregivers^24,25; occupational,²⁶ cognitive behavioral,²⁷ or family therapies^28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.^5,8

Evidence shows that recognition and diagnostic specificity of ADHD and comorbidities— not true prevalence—vary more widely among minority than among nonminority populations.

Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.²³ Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).

Continue to: Assess patients' needs and the resources available

Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.³⁰ Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.

Steps to ensuring health care equity

Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.³¹ In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,³² contributing to the 23% of children with ADHD who receive no treatment at all.²

Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.^2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.³¹ In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.

Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.

Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.⁴ Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.³³

Continue to: Impact of the COVID-19 pandemic

Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.^34,35

However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)

THE CASE

During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.

The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).

The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and ­parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.

After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed ­extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.

By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.

CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; [email protected]