Pediatricians may not be able to fix racial inequality, but they certainly can and should play a role in advocating for changes, according to a recent policy statement from the American Academy of Pediatrics.

, addresses the impact of racism on the health of children and teenagers, noting that pediatricians should always be watching for opportunities to talk to parents and patients about the effects that exposure to racism could have. Although there have been improvements in racism, as the policy statement notes, clinicians have to realize the extent to which the problem still exists.

“I have been working in this area for some time so the content doesn't surprise me, however, I think the depth of the existing data across medical, psychological, educational, and judicial and general historical literature already exists,” says Maria Trent, MD, MPH, professor of pediatrics in adolescent/young adult medicine at Johns Hopkins Medicine in Baltimore, Maryland, and co-author of the policy statement.

The goal of the policy statement was to provide evidence-based guidance on the role of racism in child and adolescent development as well as health outcomes, and to help pediatricians understand their role in employing strategies that can optimize care and improve the health and well-being of the affected children and their families. This also means examining one’s own biases, the statement notes.

“We hope that pediatricians will examine their own biases; begin to help families unpack the impact that racism is having on the health of children; and provide effective support and anticipatory guidance that results in optimal patient-centered, family engaged care, that the overall quality of care for patients and families improves, and that patients will have optimal outcomes,” Trent says. “This will require partnership with community agencies and effective advocacy not only in the office but in our local communities and beyond.”

Some suggested interventions that pediatricians can use to help patients who experience racism include the creation of a culturally safe medical home that is sensitive to racism, using strategies like Raising Resisters to provide support for children and their families to recognize and resist racism, training clinical staff to provide culturally competent care, assessing patients for stressors and connecting them and their families to community support organizations, watching for other mental health conditions-such as posttraumatic stress, anxiety, and depression-in victims of racism, and encouraging cultural diversity and community involvement in the practice.

Trent simplifies these interventions, suggesting that providers adopt the approach recommended by 

Acts of racism affect all children, teenagers, and families, and in all of the places they spend their time-including schools, Trent notes. Clinicians have to understand the impact to help, and are being tasked to proactively address racism as care providers, community leaders, and child advocates.

“The emotional and physical health impacts are both in the present and in the future,” Trent says. “The Academy is committed to facilitating strategies to optimize our workforce to be prepared to assist patients and families struggling with the short- and long-term impacts of racism in its multiple forms through its policies, publications, and programming. Most importantly, we are committed to listening to children, adolescents, and families using a culturally competent, patient-centered, family engaged approach to begin the process of healing and change.”

A study out of Stanford on racial and ethnic disparities in neonatal intensive care units

 (NICU) accompanied the policy statement, and reveals that minority infants-particularly African-American infants-were often disadvantaged when it came to care and outcome measures in NICUs. The study reviewed 41 articles which revealed widespread and complex disparities in the structure, process, and outcome measures faced by disadvantaged infants in NICUs. Its authors hope the study provides motivation to create a new normal for these children.

“This review should be seen as an invitation for providers, NICUs, hospitals, and health systems to do quality improvement through a racial/ethnic equity lens,” says Krista Sigurdson, PhD, assistant adjunct professor of social and behavioral sciences at the University of California, San Francisco and lead author of the report.

At the same time, studies are geographically/historically contextual, she notes.

“Each area of care and healthcare system merits its own analysis. One area that stands out from the systematic review is that NICUs with higher volume black infants may provide worse quality of care,” Sigurdson says. “This suggests that health systems used by black communities deserve particular quality improvement and the same may apply to pediatric services in general.”

Sigurdson says she hopes the report will result in reflection by health systems, but also action from pediatricians.

“Pediatricians can educate themselves on systemic and interpersonal racism and how preterm birth and healthcare systems-including neonatal care-exist within these larger historical and contemporary forces,” she says.

She also suggests pediatricians take a role in helping to develop quality improvement projects that partner with affected communities of color to help define problems and develop solutions tailored to addressing racial and ethnic inequalities in neonatal care. As a frontline provider to patients affected by these disparities, pediatricians can play a vital role in helping to mitigate early exposure to racism.

“In their day-to-day work, pediatricians can advocate for families of color in the NICU and outside to help ensure that they have the supports and services needed,” Sigurdson says. “Pediatricians can make sure that families know what is available to them, particularly in terms of fostering their involvement in the care of their hospitalized infant. They can trust families of color when they voice problems or have complaints about healthcare systems or providers and help address problems that arise.”

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Although progress has been made, racial and ethnic inequalities remain in medical care, but pediatricians can help to change this, as well as mitigate the damage that has already been done.

How racial inequality affects health and healthcare

For children with severe asthma, management of the disease can be more difficult, particularly in how well these patients respond to bronchodilators, according to a recent report.

 revealed that children with severe asthma have lower lung function-or predicted FEV

%-and poorer asthma control than children with more moderate asthma. This information, however, can offer clinicians new tools to help their patients manage asthma and hopefully prevent exacerbation.

Andrea Coverstone, MD, pediatric pulmonologist and professor of pediatrics at Washington University in St. Louis, Missouri, and lead author of the report says it’s important for pediatricians to be aware that bronchodilator response in patients with asthma can be used not only as a diagnostic tool, but also as a clinical tool for assessing asthma severity.

“The maximal bronchodilator response is associated with more asthma exacerbations and hospitalizations at baseline, as well as lower lung function and worse asthma control at 1-year follow-up,” she says.

Researchers analyzed the characteristics associated with reversibility of airflow obstruction and response to maximal bronchodilation in children aged 6 to 17 years who were enrolled in the National Heart, Lung and Blood Institute’s Severe Asthma Research Program (SARP). Lung function is a predictor of bronchodilator response in children with asthma, according to the report, and bronchodilator response can be used to identify a phenotype of pediatric asthma with particularly low lung function and poor asthma control.

In the study, participants with diagnosed asthma were evaluated for multiple allergens, and had serum immunoglobulin testing completed. Researchers tested fractional exhaled nitric oxide (FeNO) and performed spirometry, calculating bronchodilator reversibility as ≥12% FEVâ from their baseline. These maximum relative increases were found to be significantly higher in children with severe asthma than in those with non-severe asthma. Secondhand smoke exposure and FeNO were associated with higher reversibility after bronchodilators were given, and a higher prebronchodilator FEVâ% was associated with lower odds. Additionally, for the entire cohort, bronchodilator reversibility was associated with neutrophil counts, immunoglobulin E, and predicted FEVâ%.

The study is important because it may help identify children with asthma who may be at risk of having airflow obstruction reversibility after maximal bronchodilator administration. Coverstone says the study highlights the benefit of bronchodilator response testing as a clinical tool for ongoing care.

“While it is recommended to monitor lung function at least annually in patients with asthma, it is not common practice to routinely assess the bronchodilator response outside of the initial assessment when diagnosing asthma,” she says. “This study identifies the bronchodilator response as another tool for phenotyping asthma in children.”

Coverstone says the longitudinal findings of the report surprised her most.

“Children with a 12% bronchodilator response at their baseline assessment had less decline in lung function at 1 year compared to those that did not have a bronchodilator response; however, they also had lower lung function at initial assessment and despite having less decline, lung function remained lower at that 1 year follow-up assessment,” she says.

Coverstone suggests that long follow-up may help determine the trajectory of lung function in children with severe asthma.

“Is having a bronchodilator response indicative of the lung’s capability of preserving lung function? It appears that the bronchodilator response can be an indicator of a more severe asthma phenotype with lower lung function and asthma control, but also might indicate those more likely to respond to treatment,” she says. “Other studies have shown that a bronchodilator response is associated with a positive response to treatment with inhaled corticosteroids.”

Pediatricians should consider regularly assess bronchodilator response in their severe asthma patients to help in assessing their condition and their response to treatment, she adds. Additionally, practitioners should be aware of differences in asthma management at different severity levels, and be aware of other exposures patients have that may exacerbate their condition, like cigarette smoke exposure.

“It is important to note that children with less severe asthma often do not achieve the same level of bronchodilator response to lower doses of albuterol than those with severe asthma, and that the baseline lung function is strongly associated with the response to bronchodilators,” she says. “In clinical practice, using higher doses of albuterol may be useful in assessing the maximal response in combination with the use of FeNO, which is also associated with bronchodilator response. Assessing for smoke exposure in the home is a must.”

Bronchodilator response may offer a signal to pediatricians on the severity of a patient’s asthma, and can be used to help manage the condition.

How bronchodilators can help assess asthma severity

­The American Academy of Pediatrics (AAP) Subcommittee on Fluid and Electrolyte Therapy issued a new guideline on intravenous (IV) maintenance fluid therapy last year that was a departure from 6 decades of practice. The rationale behind those changes was discussed in depth at the 2019 AAP National Conference in New Orleans, Louisiana, at a session presented on October 27, 2019  and repeated on October 28, 2019.

Leonard Feld, MD, PhD, MMM, CPE, FAAP, clinical professor of pediatrics at the Herbert Wertheim College of Medicine at Florida International University in Miami and chair of the AAP subcommittee, led a session titled, “Water and Salt: New AAP Clinical Practice Guideline for the Maintenance of Intravenous Fluids in Children,” to discuss the 2018 “Clinical Practice Guideline: Maintenance Intravenous Fluids in Children.”

clinical practice guideline was published

 in December 2018, and the recommendation was for patients aged 28 days to 18 years in need of maintenance IV fluids to receive isotonic solutions with appropriate potassium chloride and dextrose. This recommendation has the potential to significantly reduce the risk of developing hyponatremia, according to the guideline. This is a change from 60 years of practice in favor of hypotonic fluids in these populations.

“Our objective, as stated in the article, was to provide an evidence-based approach for patients who are hospitalized and in need of IV maintenance fluids,” Feld says. “This was a very methodical approach to arrive at the recommendation, and I think it’s important to point out the guideline does not address deficit fluid therapy, or the rate at which fluids need to be delivered. We are not proposing the amount of potassium or the potassium concentration in IV fluids. We are not addressing treatments for various electrolyte abnormalities. We are also not recommending how frequently biochemical monitoring is performed.”

The recommendation was based on randomized clinical trials and took into account study biases. Feld says the recommendation is important, but recognizes the limitations of the guidance. “The recommendation to use the isotonic fluids for maintenance therapy does not mean there are no indications for administering hypotonic fluids, or that isotonic fluids will be safe in all children,” he says, noting that clinical decision-making is key in all cases. “We need to emphasize that it doesn’t apply to all children such as those with high-risk disorders such as congenital heart disease, cancer, etc...”

The committee was made up a vast spectrum of specialties, Feld says, including nephrologists, epidemiologists, hospital medicine physicians, critical care physicians, surgeons, anesthesiologists, family medicine physicians, and emergency physicians.

“Each clinician has to appropriately assess the child to decide if they need maintenance IV fluids, or if they have conditions or disease states where other fluids choices may be appropriate,” he says, adding that consultations with other specialties may be a part of the decision-making process.

Feld says he welcomed discussion about the guideline at the conference.

“This is not the end, but it opens further discussion for a continued investigation,” Feld says. “I think any guideline you publish should have a meaningful discussion. It helps achieve the understanding of how the decision was reached.”

Expert discusses the rationale on shift from 60 years of practice regarding intravenous (IV) maintenance fluid therapy.

How new IV maintenance fluid recommendations change decades of practice

Teenagers with attention-deficit/hyperactivity disorder (ADHD) or parent-reported “trouble staying focused” are poorer drivers and make more driving errors than their peers during the teenagers’ learning permit period.­ These findings are based on an analysis of survey data from a prior randomized study in which 512 parent-teenager pairs were randomized to a web-based parent-teenager driving plan intervention or a usual practice control condition for 24 weeks during the learner’s permit period and were surveyed several times, including at the end of the study period.

Of the 134 adolescents who also underwent on-road driving assessments at 24 weeks and had complete survey data, 113 (84.3%) were typically developing (TD) adolescents, 12 (9.0%) had ADHD, and 9 (6.7%) had trouble staying focused. Sociodemographic variables were similar for all 3 groups. Overall, TD teenagers did better behind the wheel than did adolescents with ADHD or those who had difficulty staying focused.

Specifically, teenagers who had difficulty staying focused were more likely than those with ADHD or TD to have their on-road driving assessment (administered by a certified driver rehabilitation specialist) terminated because the specialist had to intervene to prevent a collision, the driver violated a traffic law, or because of another serious driver action or inaction. In addition, teenagers who had difficulty staying focused received marginally lower overall driving scores compared with TD teenagers, whereas those with ADHD made significantly more total errors than TD teenagers. As for specific tasks, teenagers with ADHD made more errors during high-demand tasks and right-turn tasks compared with TD teenagers, whereas teenagers with trouble staying focused made more errors during “straight at intersection tasks.”

Teenagers with trouble staying focused and those with ADHD also committed the most so-called critical errors, most often dangerous maneuvers, followed by disobeying traffic signs, lane violations, speeding, or striking an object or curb (Bishop HJ, et al. 

The authors also comment that no specific programs are available to help drivers with ADHD improve. Teenaged drivers, with or without ADHD, remain a concern. Just remember that a license says the state feels a child can drive, but the parents still need to decide if a child should drive. You’ll find that 

Teenagers with attention-deficit/hyperactivity disorder (ADHD) or parent-reported “trouble staying focused” are poorer drivers and make more driving errors than their peers during the teenagers’ learning permit period according to recent survey data.

Learning to drive poses extra risks for teens with attention problems

Palivizumab appears to be effective for reducing respiratory syncytial virus (RSV) in high-risk infants, according to results of a study in Australia. Researchers conducted a retrospective  birth cohort study of more than 23,000 high-risk infants admitted to neonatal intensive care units who were born from 2002 to 2013 with follow-up to 2015. To address confounding by indication in the cohort study (ie, that palivizumab was targeted to those at greatest risk of RSV), researchers supplemented this analysis with a self-controlled case series (SCCS) study.

In the cohort group, 1.1% of the infants received at least 1 dose of palivizumab, with use increasing over time. The number of doses ranged from 1 to 15, and more than 90% of them were administered to infants aged younger than 12 months. Overall, there were 1689 positive RSV tests before the age of 2 years, representing 1506 infants (6.2%) with at least 1 RSV detection before age 2 years. More than 10% of these infants also had another episode of RSV detection before their second birthday. Overall, receiving palivizumab was not associated with lower risk of RSV detection before age 2 years.

However, results of the SCCS study, which accounted for confounding by indication and focused on 1506 infants with 1 or more RSV detections who had at least 1 dose of palivizumab, were different. The incidence of RSV detection before age 2 years was 70% lower in the 28 days after the first dose of palivizumab than it was in control periods, and the rate of RSV detections was reduced by 74% in the 28 days after any dose (

I have never been completely convinced that palivizumab is worth the cost, yet I prescribe it. This study, although hardly conclusive, makes me feel better about giving it.

Palivizumab appears to be effective for reducing respiratory syncytial virus (RSV) in high-risk infants, according to results of a study in Australia.

Study confirms effectiveness of palivizumab against RSV in high-risk infants

A study in 512 mother-child pairs from 6 major cities in Canada found that exposure to higher levels of fluoride during pregnancy was associated with lowered intelligent quotient (IQ) scores in their children at the age of 3 to 4 years.

About 41% of participants lived in communities supplied with fluoridated municipal water. Investigators matched participants’ postal codes with water treatment plan zones to estimate water fluoride concentration for each woman. Using a questionnaire, they determined mothers’ consumption of tap water, coffee, and tea during the first and third trimesters and measured maternal urinary fluoride (MUF) concentration in each trimester of pregnancy. They assessed children’s IQ when they were aged 3 or 4 years, using standardized tests.

As expected, median MUF concentration was significantly higher among women who lived in communities with fluoridated drinking water, as was their daily estimated fluoride intake, compared with those who did not live in such communities. Analyses showed that an estimated 1-mg increase in maternal fluoride intake was associated with a 3.66 lower IQ score among both boys and girls. A 1-mg/L increase in MUF was associated with a 4.49-point lower IQ score in boys but not in girls (

I do not like giving anti-fluoride spouters ammunition, but I have to follow science where it leads. The reviewers and editors were very brave to publish this controversial study. We will see if it is replicated down the road. The study looked only at pregnant women, so continue to give fluoride, a well-proven treatment, to your pediatric patients who need it.

Fluoride exposure in pregnancy can affect offspring’s IQ

A healthy 6-year-old boy presents for evaluation with a 3-month history of an asymptomatic rash extending from his left thumb to his left wrist (Figure).

Lichen striatus is an uncommon condition that usually affects children aged to 15 years. It often presents as a linear band of inflammatory flat-topped papules ranging in color from pink to skin-colored to tan and often resolves with postinflammatory hypopigmentation. The linear arrangement of the papules characteristically follows Blaschko’s lines and can present in a continuous band or with interrupted areas. The distribution along Blaschko’s lines points to a somatic mosaicism pathogenesis, but neither the involved genes nor the inciting factors are known.

 The papules tend to be asymptomatic but occasionally have associated pruritis.

Lichen striatus usually appears on the extremities and less commonly on the trunk, face, neck, or buttocks. Lichen striatus rarely affects the nail, but when it does it is almost exclusively seen in children. Unlike lichen planus that can affect the whole nail, lichen striatus involves just the medial or lateral portion and may result in onycholysis, splitting, longitudinal ridging, fraying, or, rarely, total nail loss.

The condition tends to appear abruptly and reaches its maximum extent within a few days to weeks (occasionally up to several months), then spontaneously resolves over a period of a few months to 2 to 3 years. The resulting postinflammatory hypopigmentation can take a year or more to disappear. In individuals with darker skin tones, lichen striatus may not be noticeable until the appearance of a resolving band of hypopigmentation.

 Recurrences of lichen striatus are unusual.

The histological findings of lichen striatus can vary depending on which part of the linear band is biopsied, and how long the lesion has been present.

 However, most cases display a combination of spongiotic and lichenoid interface dermatitis with perivascular and periadnexal lymphocytic infiltrate present in the dermis.

 The infiltrate can surround eccrine sweat glands, ducts, and hair follicles distinguishing it from lichen planus.

Epidermal changes include hyperkeratosis, focal parakeratosis, intercellular and intracellular edema, focal spongiosis, and lymphocytic exocytosis.

 Dyskeratotic keratinocytes also can be found in the granular and horny layers or at the level of the dermoepidermal junction.

The differential diagnosis includes linear lichen planus (LP), blaschkitis, linear graft versus host disease (GVHD), linear epidermal nevus, lichen nitidus, and other inflammatory disorders in a linear pattern such as linear porokeratosis, and linear psoriasis. Blaschkitis more often favors the trunk, has multiple streaks, and presents in adults,

 and linear GVHD occurs in a specific clinical setting. Although lichen striatus and linear LP can look similar histologically, their clinical appearance is what sets them apart. Hypopigmentation is the most common sequala of lichen striatus, whereas linear lichen planus resolves with hyperpigmentation.

 If lichen striatus persists beyond a year’s time, a biopsy can help distinguish lichen striatus from other entities.

Lichen striatus is a benign, transitory condition not requiring treatment unless the lesion is pruritic, in which case topical steroids or nonsteroidal antiinflammatory agents such as calcineurin inhibitors can be prescribed.

For this patient, lichen striatus was diagnosed clinically and no further workup was required. The natural history of the disease was discussed with the family, and they elected to have the boy followed clinically without treatment.

1. Shiohara T, Kano Y. Lichen planus and lichenoid dermatoses. In: Bolognia J, Jorizzo J, Schaffer J, eds. 

. 3rd ed. Philadelphia: Elsevier/Saunders; 2012:183-202.

2. Tilly JJ, Drolet BA, Esterly NB. Lichenoid eruptions in children. 

3. Graham JN, Hossler EW. Lichen striatus. 

4. Mu EW, Abuav R, Cohen BA. Facial lichen striatus in children: retracing the lines of Blaschko. 

5. Goyal S, Cohen BA. Pathological case of the month. Lichen striatus. 

A healthy 6-year-old boy presents for evaluation with a 3-month history of an asymptomatic rash extending from his left thumb to his left wrist. What's the diagnosis?

Linear papules appear on a boy’s thumb, wrist

Although many parents report food allergy in their children and the incidence of parental report has increased over time,

 the actual incidence of confirmed food allergy is much lower.

 However, food allergy still is estimated to impact 2% to 10% of pediatric patients, and its prevention is an important goal in pediatric practice because there is no current cure.

The pediatrician needs to be aware of changing practice recommendations related to the introduction of complementary foods for children. Although pediatricians who have been in practice for some time may have previously asked parents to delay the introduction of highly allergenic foods, emerging evidence now suggests just the opposite. Earlier introduction of highly allergenic foods may actually prevent food allergy.

Food allergies refer to reactions that occur as a result of immunologic reactions in response to certain foods. Food allergies are generally classified as either immunoglobulin (Ig)E mediated or non–IgE mediated and have different clinical presentations.

Whereas any food can theoretically lead to an allergic reaction, the most common offenders are:

Immunologic IgE-mediated reactions may present with the following symptoms:

·      Gastrointestinal anaphylaxis

Non–IgE-mediated food allergies are more likely to present with subacute, chronic symptoms that are isolated to the gastrointestinal tract or skin.

Based on the idea that delaying exposure to solid foods might prevent atopic dermatitis and other allergic disease, the American Academy of Pediatrics (AAP) recommended in 2000 that children at high risk for developing food allergies delay the introduction of certain foods

: delay cow’s milk until age 1 year; eggs until age 2 years; peanuts, tree nuts, and fish until age 3 years. Although not specifically recommended, many pediatricians incorporated these guidelines into their routine recommendations in some form or fashion for other lower-risk children.

In 2008, the AAP updated its policy statement that included recommendations for the prevention of atopic disease. The report concluded that there was insufficient data and evidence to justify delaying the timing of complementary foods beyond the age of 4 to 6 months and that there was no protective effect of any dietary intervention beyond this age impacting the development of atopic disease.

 the AAP summarizes additional research since the 2008 report, concluding that there is no evidence that delaying the introduction of highly allergenic foods such as peanuts, eggs, and fish beyond age 4 to 6 months prevents atopic disease.

 The report goes on to cite evidence that early introduction of peanuts may prevent peanut allergy.

The Learning Early About Peanut (LEAP) study was the first randomized controlled trial (RCT) to show that early exposure to peanut could prevent peanut allergy in high-risk infants.11 The authors believe that early exposure to peanut in the environment (ie, skin) leads to sensitization while early dietary exposure may lead to immune tolerance.

In this study, high-risk infants from the United Kingdom (UK), defined as having severe eczema, egg allergy, or both, were randomized into 2 groups of peanut exposure and then stratified based on pinprick testing (children with a response greater than 4 mm were excluded): early (aged between 4 and 11 months), or delayed (avoidance until age 5 years).

Only 1.7% of participants with early peanut exposure developed peanut allergy after age 5 years whereas 13.7% of participants randomized to avoidance as a prevention strategy developed peanut allergy. The 11.8% absolute difference in risk of peanut allergy (95% confidence interval [CI], 3.4-20.3; 

<0.001) represents a greater than 85% relative risk (RR) reduction. The LEAP study demonstrated that early peanut exposure decreases peanut allergy in both sensitized infants and nonsensitized infants.

In a follow-up study known as LEAP-On, both the avoidance and consumption groups were asked to avoid peanut for 1 year at the conclusion of LEAP. Peanut allergy continued to be more common in the original avoidance group compared with the early exposure group (18.6% vs 4.8% of children, respectively; 

Early introduction of peanut was also found to prevent peanut allergy in the Enquiring About Tolerance (EAT) RCT.

 In this study, exclusively breastfed infants were randomized to receive early introduction of peanut or 5 other allergenic foods (cooked egg, cow’s milk, sesame, whitefish, or wheat) at age 3 months, or continue exclusive breastfeeding until age 6 months. Infants in the early introduction group were less likely to develop peanut allergy compared with children randomized to UK Department of Health advice to delay food introduction to age 6 months (0% vs 2.5%, respectively; 

=0.003). A meta-analysis of the LEAP and EAT studies determined with “moderate certainty” that early introduction of peanut decreased the risk of peanut allergy (RR, 0.29; 95% CI, 0.11-0.74).

In 2017, the National Institute of Allergy and Infectious Diseases (NIAID)-sponsored expert panel on peanut allergy issued a 3-tiered recommendation for the introduction of peanut into an infant’s diet. The guideline provides the option for assessments that may be performed in a primary care practice or for referral for specialty care (Table).

Six RCTs have been published since 2008 looking at the introduction of egg to prevent egg allergy.

One example is the Prevention of Egg Allergy with Tiny Amount Intake (PETIT) study.

 The PETIT study, which was stopped early due to benefit, demonstrated that ingesting heated egg powder daily from age 6 months lowered the rate of egg allergy compared with infants who avoided egg completely until age 1 year (9% vs 38%, respectively; 

Although there are differences in these studies related to the types of patients enrolled, mechanisms used to prevent allergy, and in the assessed outcomes/results that can make drawing conclusions difficult,

 Ierodiakonou and colleagues performed a meta-analysis of 5 studies that included nearly 2000 infants and found “moderate certainty” that introduction of egg between age 4 to 6 months reduced the risk of egg allergy (RR, 0.56; 95% CI, 0.36-0.87).

The pediatrician needs to be aware of changing recommendations and the changing environment for the prevention of food allergy. With significant changes in recommendations over the last 20 years and more likely to come over the next several years, the pediatrician must examine his or her current recommendations for the introduction of highly allergenic foods into a child’s diet based on that child’s risk and determine how he or she will communicate these changes to parents going forward.

1. Peters RL, Koplin JJ, Gurrin LC, et al; HealthNuts Study. The prevalence of food allergy and other allergic diseases in early childhood in a population-based study: HealthNuts age 4-year follow-up. 

2. Verrill L, Bruns R, Luccioli S. Prevalence of self-reported food allergy in U.S. adults: 2001, 2006, and 2010. 

3. Venter C, Pereira B, Grundy J, et al. Incidence of parentally reported and clinically diagnosed food hypersensitivity in the first year of life. 

4. EggesbÃ¸ M, Botten G, Halvorsen R, Magnus P. The prevalence of CMA/CMPI in young children: the validity of parentally perceived reactions in a population-based study. 

5. Chafen JJ, Newberry SJ, Riedl MA, et al. Diagnosing and managing common food allergies: a systematic review. 

6. Du Toit G, Sampson HA, Plaut M, Burks AW, Akdis CA, Lack G. Food allergy: update on prevention and tolerance. 

7. Burks AW, Tang M, Sicherer S, et al. ICON: food allergy. 

8. Committee on Nutrition; American Academy of Pediatrics. Hypoallergenic infant formulas. 

9. Greer FR, Sicherer SH, Burks AW, American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Allergy and Immunology. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. 

10. Greer FR, Sicherer SH, Burks AW; Committee on Nutrition, Section on Allergy and Immunology. The effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, hydrolyzed formulas, and timing of introduction of allergenic complementary foods. 

11. Du Toit G, Roberts G, Sayre PH, et al; LEAP Study Team. Randomized trial of peanut consumption in infants at risk for peanut allergy. 

. 2015;372(9):803-813. Erratum in: Randomized trial of peanut consumption in infants at risk for peanut allergy. 

12. Du Toit G, Sayre PH, Roberts G, et al; Immune Tolerance Network LEAP-On Study Team. Effect of avoidance on peanut allergy after early peanut consumption. 

13. Perkin MR, Logan K, Tseng A, et al; EAT Study Team. Randomized trial of introduction of allergenic foods in breast-fed infants. 

14. Ierodiakonou D, Garcia-Larsen V, Logan A, et al. Timing of allergenic food introduction to the infant diet and risk of allergic or autoimmune disease: a systematic review and meta-analysis. 

15. Togias A, Cooper SF, Acebal ML, et al. Addendum guidelines for the prevention of peanut allergy in the United States: summary of the National Institute of Allergy and Infectious Diseases-sponsored expert panel. 

16. Palmer DJ, Metcalfe J, Makrides M, et al. Early regular egg exposure in infants with eczema: a randomized controlled trial. 

17. Bellach J, Schwarz V, Ahrens B, et al. Randomized placebo-controlled trial of hen’s egg consumption for primary prevention in infants. 

18. Palmer DJ, Sullivan TR, Gold MS, Prescott SL, Makrides M. Randomized controlled trial of early regular egg intake to prevent egg allergy. 

19. Wei-Liang Tan J, Valerio C, Barnes EH, et al; Beating Egg Allergy Trial (BEAT) Study Group. A randomized trial of egg introduction from 4 months of age in infants at risk for egg allergy. 

20. Natsume O, Kabashima S, Nakazato J, et al; PETIT Study Team. Two-step egg introduction for prevention of egg allergy in high-risk infants with eczema (PETIT): a randomised, double-blind, placebo-controlled trial. 

21. Perkin MR, Bahnson HT, Logan K, et al. Association of early introduction of solids with infant sleep: a secondary analysis of a randomized clinical trial. 

22. Fleischer DM, Spergel JM, Assa’ad AH, Pongracic JA. Primary prevention of allergic disease through nutritional interventions. 

23. Section on Breastfeeding. Breastfeeding and the use of human milk. 

Emerging evidence reveals that earlier introduction of highly allergenic foods into infants’ diets may actually lead to immune tolerance. Here’s what you should know.

New evidence changes guidelines for food allergies

An 8-year-old, previously healthy girl presents to the emergency department (ED) with a rash “that looks likes bruises” and joint pain (Figure). Her mother reports that the rash started over her daughter’s lower legs a week earlier and has since spread to her thighs and buttocks. The red patchy rash is not painful and not pruritic. The girl denies new exposures to food or topical products, recent travel, camping, or recent injury.

There is no previous history of easy bleeding or bruising. Both patient and mother deny abuse. No other family members have a similar rash. The patient also reports a 2-day history of new onset left knee and left ankle pain associated with knee swelling, which has since spontaneously resolved. No recent trauma is noted.

The patient denies swelling of her hands or shoulders. She denies chest pain, abdominal pain, dysuria, or hematuria. A week prior to the rash, she was evaluated for fever and sore throat and tested negative for streptococcal infection.

On exam, the child is well appearing, alert, and hydrated. Her weight is 87 lb (98th percentile); temperature is 98.5°F; pulse is 98; respiratory rate is 24 breaths/min; blood pressure is 110/60 mm Hg; and pulse oximetry is 100% on room air.

Her physical exam is negative for conjunctivitis, oral ulcers, or lymphadenopathy. Respiratory and cardiovascular exams are within normal limits. Abdominal exam is negative for tenderness on palpation without guarding or rigidity, and bowel sounds are normal. No hepatosplenomegaly is palpated.

The ankle joints are tender on palpation over the lateral and medial malleolus without any swelling, erythema, deformity, or restriction of motion. The knee and hip joints are normal. Neurologic exam is normal without any focal neurologic defects identified.

Her skin exam is positive for palpable purpuric rash that is nonblanchable and nontender (Figure). She also has an interspersed petechial rash over the lower extremity that extends from the ankles to the thighs, lower abdomen, and buttocks. The soles of her feet are not involved.

Initial blood work revealed a complete blood count (CBC) with a slightly elevated white blood cell (WBC) count of 10.5 X 109 /L (3.40-9.5 X 109/L) with a normal differential; hemoglobin, 12.9 g/dL (12-14 g/dL); platelet count of 481 X 10 9/L (150-450 X 109/L). A complete metabolic panel showed normal liver function tests and a normal urea/creatinine ratio. Urinalysis was negative for protein, blood, or leukocytes. Serum antinuclear antibody (ANA) test was negative.

The differential diagnosis for rash with joint pain in children is broad and includes both infectious and noninfectious causes (Table). A detailed history with pertinent positives and negatives and a thorough exam is helpful in making the diagnosis. Some of the common differentials are discussed below.

 is a multisystem autoimmune condition caused by inflammation of the blood vessels and connective tissue. Because this condition can involve multiple systems of the body and occurs in episodic flares, the periodic constellation of symptoms can make it hard to diagnose.

Generalized symptoms such as fever, weight loss, lymphadenopathy, and hepatosplenomegaly along with the classic malar rash and nonerosive symmetric arthritis should raise the suspicion for SLE. Laboratory workup is usually positive for cytopenias, transaminitis, and elevated inflammatory markers. A positive ANA titer is a very sensitive marker but not specific, and in the event that it is positive, follow-up with specific anti–double-stranded DNA (anti-ds-DNA) antibody and anti-smith (Sm) antibody should be done to differentiate SLE from other connective tissue and vascular disorders.

The patient in this case was well appearing without systemic symptoms and had both a normal blood count and a negative ANA, which made SLE less likely.

 the pathognomic of the early localized stage (most common presentation within the first 1 to 4 weeks after a tick bite) is the erythema migrans (EM) rash, which appears as a “target-like lesion” or “bull’s-eye appearance” and can be found on the abdomen, axilla, inguinal, or popliteal areas. This is associated with systemic signs such as fever, arthralgia, and headaches.

Laboratory studies might show leukopenia or leukocytosis, elevated inflammatory markers such erythrocyte sedimentation rate (ESR), and liver function abnormalities. Early disseminated disease secondary to hematogenous spread of the bacteria presents as multiple EM, neurologic involvement including facial nerve palsy, or carditis. Lyme arthritis is the main symptom of late disseminated disease, presenting months to years after the tick bite. Lyme disease can be monoarticular or oligoarticular with small effusions and absence of fever.

No exposure to the tick and absence of the characteristic rash and laboratory abnormalities made this diagnosis less likely in this patient.

 is one of the causes of primary acquired heart diseases due to an inflammatory reaction after a streptococcal infection. It is a clinical syndrome that includes criteria as outlined in the Jones criteria.

 Laboratory evidence of a preceding group A streptococcal infection is mandatory for the diagnosis. The rash associated with ARF is erythema marginatum, which is a macular blanching rash characterized by central clearing and found mostly on the trunk and proximal extremities. Migratory polyarthritis and carditis are the most common presenting symptoms.

The rash in this patient did not match the description of the classic rash seen with ARF and her rapid strep test was negative. Since the suspicion for ARF was low based on clinical findings, a throat culture was not ordered.

Idiopathic thrombocytopenic purpura (ITP)

 is an autoimmune condition resulting in increased platelet destruction secondary to antiplatelet antibodies. It is the most common cause of isolated thrombocytopenia in otherwise well children. It can manifest as sudden onset bruising, petechiae, or mucosal hemorrhage, usually after a viral upper respiratory infection and rarely after live vaccinations. On physical exam, lymphadenopathy might be present secondary to the viral infection, but other systemic signs are absent. Isolated low platelet count below 50 X 103/Î¼L with an elevated mean platelet volume and a normal hemoglobin and total white cell count is the only significant laboratory finding. Most cases are self-limiting within 1 to 4 weeks and treatment with oral steroids, intravenous immunoglobulin (IVIG), or anti-D IG is reserved for children with severe hemorrhage or platelet count less than 20 X 103/Î¼L.

Normal platelet count ruled out ITP in this patient.

Henoch-Schonlein purpura (HSP) is an immune-mediated, small-cell vasculitis and can mimic different conditions depending on the system involved: Abdominal pain secondary to gastrointestinal (GI) involvement can present as acute abdomen; joint involvement may mimic juvenile idiopathic arthritis (JIA), rheumatic arthritis, or gonococcal arthritis; and the rash can look similar to ITP, rickettsial diseases, sepsis, or disseminated intravascular coagulation. Laboratory tests are nonspecific for HSP, and more useful is ruling out other potential causes of the presenting symptoms.

Given the characteristic purpuric rash in this otherwise well-appearing patient, along with laboratory findings ruling out the other potential causes, a diagnosis of HSP was made.

Henoch-Schonlein purpura is the most common systemic small-vessel vasculitis in children.

 The mean age of presentation is 6 to 10 years, and the incidence is known to be equal in boys and girls. The disease is more common in autumn and spring.

The classical pathogenic feature of HSP is deposition of IgA immune complexes in the vessel walls of the kidney and other affected organs. These in turn activate the complement pathway that triggers the inflammatory cascade leading to the clinical picture discussed. The most common trigger for HSP is known to be upper respiratory infection.

 Several other viruses and bacteria including but not limited to influenza, parainfluenza, Epstein-Barr virus (EBV) and 

There have been associations of certain vaccinations such as influenza, meningococcal, measles/mumps/rubella (MMR), and pneumococcal as well as certain drugs with the onset of HSP. However, these associations have not been proven to be linked to causality, and in most cases such associations have been presumed coincidental.

The diagnosis of HSP is clinical and based on palpable purpura along with one of the following features:

3. Renal involvement with proteinuria or hematuria; or

4. Renal biopsy with predominant IgA deposition with leukoclastic vasculitis.

Skin rash in HSP has been described as petechial or palpable purpura. The rash is symmetrical, nontender, and most commonly observed on the extensor surfaces of the dependent portions of the lower extremities and the buttocks. Involvement of the abdomen and face have been described in rare cases.

 Hemorrhagic bullae have been reported in only 2% of the affected children and are not related to the severity or the progression to renal failure.

 In some cases, macular and urticarial rashes have been reported prior to the development of the purpuric rash.

Abdominal pain is the most common (~75%) associated symptom secondary to visceral purpura causing bowel edema and hemorrhage. Colicky diffuse pain, which is worse after meals and that may be associated with emesis, hematemesis, or guaiac positive stool, is the most common presentation. Although it is associated with purpura the majority of the time, abdominal pain may precede the classic rash in less than 40% of the cases, thereby making the diagnosis a challenge.

 Intussusception is the most common complication of abdominal involvement, and an ultrasound is the initial diagnostic modality for identifying it. More severe complications such as extensive hemorrhage and bowel wall gangrene are rare.

Arthritis/arthralgia is the presenting symptom in approximately 25% of patients with HSP, however, more than 50% of patients have articular involvement.

 It is usually oligoarticular and involves the larger joints of the lower extremities. Even though the pain, swelling, and restricted range of movement can cause significant discomfort, the symptoms resolve spontaneously within a few days to weeks and the response to nonsteroidal anti-inflammatory drugs (NSAIDs) is well documented. There is no longterm deformity or chronic damage to the joints or ligaments.

Renal involvement is seen in 20% to 50% of the patients diagnosed with pediatric HSP.

 The earliest finding is microscopic hematuria with or without proteinuria.

 Children aged older than 4 years, purpura persisting for longer than 1 month, and severe GI bleeding are higher risk factors for developing renal disease. The renal symptoms take longer to manifest in comparison with the joint and abdominal symptoms. Several studies have shown that renal involvement was apparent within 3 months of appearance of the purpura in 97% of the patients and within 4 weeks for 75% of the patients.

 Based on this, weekly urinalysis and blood pressure measurements must be performed in the first 3 months after diagnosis. About 12% of the children with HSP end up with chronic renal failure about 3 to 4 years after diagnosis.

Other clinical features that have been reported but are less common are headaches, intracranial hemorrhage, pulmonary hemorrhage, scrotal hematoma, and orchitis.

Routine blood work and imaging are not needed to diagnose HSP but may be obtained in atypical presentations in order to rule out other diagnoses. Initial investigations may include a CBC, urea, creatinine, coagulation studies, and urinalysis (UA). If the UA is positive for hematuria or proteinuria, it should be followed up with a protein/creatinine ratio and further laboratory tests to rule out other causes of glomerulonephritis. Moderate leukocytosis with a mild increase in acute phase reactants is commonly seen. Even though HSP by definition requires a normal platelet count, mild thrombocytosis may be seen in children with GI involvement. Elevated IgA levels are seen in 50% of the patients with HSP, however, it is very nonspecific and there is also no co-relation of the IgA levels with the disease severity. Complement levels are normal.

Biopsy remains the most specific diagnostic tool but is rarely indicated. It is only considered if the diagnosis is uncertain or if the patient has progressive renal disease or nephrotic range proteinuria. Leukoclastic vasculitis affecting the small blood vessels along with perivascular infiltration of neutrophils is typical.

Immunofluorescence shows with IgA deposits along with possible C3 deposits seen in the mesangial wall.

The management of HSP is primarily supportive and involves hydration and pain control with NSAIDs, and rarely with opioids. The treatment with NSAIDs has not shown to increase the risk of GI bleeding. However, in patients with renal involvement and on NSAIDs, close monitoring of renal function and blood pressure is of utmost importance.

The use of steroids in patients with HSP is controversial. Whereas some studies have shown that early use of steroids decreases the duration of abdominal pain and prevents GI and renal complications, other studies have shown no difference.

 Immunosuppressive treatment and renal biopsy are reserved for patients with nephrotic range proteinuria and progressive renal impairment. An essential part of following patients with HSP is monitoring them for complications. An abdominal ultrasound is required for patients with new onset severe abdominal pain. Any change in mental status should prompt an evaluation for intracranial hemorrhage.­

The prognosis is generally excellent with the majority of the children experiencing complete resolution of the symptoms within 2 to 3 weeks. One-third of the patients experience a recurrence, usually within the first 6 months of diagnosis.

 A recurrence is defined as reappearance of the symptoms after resolution of the disease for at least 2 weeks. It is more likely to happen in children with nephritis. The age of the patient has not been shown to have any association with recurrence risk.

Close monitoring for children diagnosed with HSP is essential. Serial urinalysis and blood pressure checks should be performed weekly for the first month, every 2 weeks until 3 months, and monthly until 6 months.

 Renal involvement suggested by hypertension or macroscopic/microscopic hematuria or proteinuria should prompt a nephrology referral. The risk of renal involvement decreases significantly after 6 months.

The patient in this case is being followed in clinic weekly for urinalysis and blood pressures, which have thus far been negative for hematuria or proteinuria. Her purpuric rash had resolved at about 2 weeks and she now has petechial rashes over the lower extremities. At 3 weeks postdiagnosis, she started complaining of intermittent abdominal pain after meals, and an ultrasound was done that was negative for intussusception. The patient will continue to be monitored as per protocol.

An 8-year-old, previously healthy girl presents to the emergency department (ED) with a rash “that looks likes bruises” and joint pain.  The red patchy rash is not painful and not pruritic. What's the diagnosis?

Vol 37 No 1