We read with interest Dr. Smee et al.’s article on surfactant administration via laryngeal mask (LMA) in infants with respiratory distress syndrome: an intriguing topic, suggesting a minimally invasive approach to ensure a well-established therapy.
The authors stated that “use of LMA to administer surfactant is feasible in infants ≥ 1200g, reducing the need for intubation and mechanical ventilation”. (1) Despite a recent meta-analysis showing that this approach may have some advantages on short term outcomes, (i.e. reduction in need for intubation and mechanical ventilation), available evidence was based on small, poor-quality studies. (2)
In addition, there are many unanswered questions on the application of this approach in neonates. It is not known which supraglottic airway device (SAD) may be best suited (there are at least 7 different types of commercially available size-1 SADs), the characteristics of the cuff (inflatable or not-inflatable) and the most appropriate size, (3,4) whether a catheter inside the mask should be used and if yes, where the catheter’s tip should be positioned (proximally or distally), under vision or blindly. There is uncertainty on whether the patient needs mild sedation, general or topical anesthesia, or nothing at all, and around the best mode to support respiratory efforts and potential complications (i.e. hypoxia or bradycardia) during the procedure. (1)
The authors also reported that “LMAs to fit the more immature infan...
We read with interest Dr. Smee et al.’s article on surfactant administration via laryngeal mask (LMA) in infants with respiratory distress syndrome: an intriguing topic, suggesting a minimally invasive approach to ensure a well-established therapy.
The authors stated that “use of LMA to administer surfactant is feasible in infants ≥ 1200g, reducing the need for intubation and mechanical ventilation”. (1) Despite a recent meta-analysis showing that this approach may have some advantages on short term outcomes, (i.e. reduction in need for intubation and mechanical ventilation), available evidence was based on small, poor-quality studies. (2)
In addition, there are many unanswered questions on the application of this approach in neonates. It is not known which supraglottic airway device (SAD) may be best suited (there are at least 7 different types of commercially available size-1 SADs), the characteristics of the cuff (inflatable or not-inflatable) and the most appropriate size, (3,4) whether a catheter inside the mask should be used and if yes, where the catheter’s tip should be positioned (proximally or distally), under vision or blindly. There is uncertainty on whether the patient needs mild sedation, general or topical anesthesia, or nothing at all, and around the best mode to support respiratory efforts and potential complications (i.e. hypoxia or bradycardia) during the procedure. (1)
The authors also reported that “LMAs to fit the more immature infants are not yet currently widely available.” To our knowledge, there are no LMAs designed to fit this smaller population. Improper use of the currently available LMAs in more immature infants may be dangerous. (5)
Despite the great enthusiasm and interest of neonatologists on this approach for surfactant administration in infants with RDS, more evidence is needed to recommend this practice. Based on currently available evidence, surfactant administration via SAD should be limited to clinical trials.
References
1. Smee NJ, O'Shea JE. Can the laryngeal mask airway be used to give surfactant in preterm infants? Arch Dis Child. 2020 Apr 7:archdischild-2019-318562.
2. Calevo MG, Veronese N, Cavallin F, Paola C, Micaglio M, Trevisanuto D. Supraglottic airway devices for surfactant treatment: systematic review and meta-analysis. J Perinatol. 2019;39:173-183.
3. Tracy MB, Priyadarshi A, Goel D, Lowe K, Huvanandana J, Hinder M. How do different brands of size 1 laryngeal mask airway compare with face mask ventilation in a dedicated laryngeal mask airway teaching manikin? Arch Dis Child Fetal Neonatal Ed. 2018;103:F271-F276.
4. Bansal SC, Caoc i S, Dempsey E, Trevisanuto D, Roehr CC. The Laryngeal MaskAirway and Its Use in Neonatal Resuscitation: A Critical Review of Where We Are in 2017/2018. Neonatology. 2018;113:152-161.
5. Trevisanuto D, Parotto M, Doglioni N, Zanardo V, Micaglio M. Upper esophageal lesion following laryngeal mask airway resuscitation in a very low birth weight infant. Resuscitation. 2011 Sep;82(9):1251-2.
Low Prevalence of Kingella kingae Infections in UK Children
Pablo Yagupsky, MD
Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Corresponding Author: Pablo Yagupsky, Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel 84101. Phone number: (972) 506264359. Fax number: (972) 86403541. e-mail: PYagupsky@gmail.com
Dear Editor:
In a recent article, Abeywickrema et al. summarized 10 years of pediatric joint and bone infections in Oxford, and concluded that Staphylococcus aureus was the most common etiology [1]. Although this concept was widely accepted in the past, the increasing use of sensitive nucleic acid amplification tests has demonstrated that Kingella kingae is the leading agent of skeletal system infections in the 6-48 month-old population, causing up to 88% of the cases in this age group [2]. Abeywickrema et al., however, isolated the bacterium in only 3 of the 74 (4%) patients in whom the etiology could be determined [1]. Kingella kingae is notoriously fastidious and the traditional culture methods and microscopy employed by the researchers are usually unable to detect its presence in joint and bone exudates [3]. Invasive K. kingae infections other than endocarditis are characterized by a mild local and systemic inflammation: fev...
Low Prevalence of Kingella kingae Infections in UK Children
Pablo Yagupsky, MD
Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Corresponding Author: Pablo Yagupsky, Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel 84101. Phone number: (972) 506264359. Fax number: (972) 86403541. e-mail: PYagupsky@gmail.com
Dear Editor:
In a recent article, Abeywickrema et al. summarized 10 years of pediatric joint and bone infections in Oxford, and concluded that Staphylococcus aureus was the most common etiology [1]. Although this concept was widely accepted in the past, the increasing use of sensitive nucleic acid amplification tests has demonstrated that Kingella kingae is the leading agent of skeletal system infections in the 6-48 month-old population, causing up to 88% of the cases in this age group [2]. Abeywickrema et al., however, isolated the bacterium in only 3 of the 74 (4%) patients in whom the etiology could be determined [1]. Kingella kingae is notoriously fastidious and the traditional culture methods and microscopy employed by the researchers are usually unable to detect its presence in joint and bone exudates [3]. Invasive K. kingae infections other than endocarditis are characterized by a mild local and systemic inflammation: fever is often absent, WBC counts in the blood and synovial fluid are frequently normal, and acute phase reactants are within the normal range or only mildly elevated, requiring a high index of suspicion and the use of sensitive detection methods for confirmation [3]. In France, Switzerland, and Israel, where molecular assays are routinely employed, the role of K. kingae as the prime osteoarticular pathogen in young children has been firmly established [2, 4], but the organism is conspicuously underrepresented in UK reports [1, 5]. I believe that many children with K. kingae disease were consistently overlooked in the study and are hidden in the culture-negative category, or were dismissed altogether as unconfirmed cases of septic arthritis or osteomyelitis [3]. It is to be expected that the increasing use of nucleic acid amplification tests will improve the laboratory diagnosis of skeletal system infections in early childhood and contribute to better patients’ management.
References
1. Abeywickrema M, Liu X, Kelly DF, et al. Bone and joint infections in Oxford: a 10-year retrospective review. Arch Dis Child 2020; 105:515-516.
2. Juchler C, Spyropoulou V, Wagner N, et al. The contemporary bacteriologic epidemiology of osteoarticular infections in children in Switzerland. J Pediatr 2018;194:190-196.
3. Yagupsky P. Kingella kingae: carriage, transmission, and disease. Clin Microbiol Rev 2015;28:54-79.
4. Chometon S, Benito Y, Chaker M, et al. Specific real-time polymerase chain reaction places Kingella kingae as the most common cause of osteoarticular infections in young children. Pediatr Infect Dis J 2007;26:377-381.
5. de Graaf H, Sukhtankar P, Arch B, et al. Duration of intravenous antibiotic therapy for children with acute osteomyelitis or septic arthritis: a feasibility study. Health Technol Assess 2017;21:1-164.
Since the introduction of the national delay phase response to Covid-19 Coronavirus in the republic of Ireland on March 12th and subsequent advise to stay at home from March 27th, essential paediatric cardiac services have had to continue in a limited capacity.
In that time, our national tertiary referral centre has seen 428 children in the out-patient's setting, 223 on the cardiac day ward, and performed an intervention (cardiac surgery or cardiac catheterization) in 140 cases. This includes 41 cardiac by-pass cases, 22 non-bypass cases, 49 interventional cardiac catheterization cases and 6 hybrid procedures involving both the cardiac surgery and cardiac catheterization teams.
Of the 49 patients screened pre-operatively, not one positive (and asymptomatic) case was identified.
Adhering to government advice on social distancing and appropriate PPE where indicated, not a single member of the extended medical team has been known to cntract Covid-19 Coronavirus from contact with patients or their families in this time.
This anecdotal case experience from one institution supports the proposal to allow children to return to school regardless of comorbidities, in recognition of the considerable long-term educational and social harm that exclusion would result in.
Munro APS & Faust SL, in their viewpoint (1) quite correctly build on the evidence of low risk of contagion and rare complications of Covid-19 infection among children to call for reopening of schools. There are, however, several other good reasons to be considered.
First, as all international agencies have highlighted, prolonged closure yields serious consequences for all children and particularly for those already living in difficult circumstances, such as extreme poverty, disability, or violent environments (2,3). UNESCO estimates that at least 177 countries have instituted school closures at national level and several other countries have established closings at regional or local level (4). With over 90% of students worldwide (more than 1.5 billion young people) currently out of the educational context, it is clear that the greatest threats from Covid-19 to children and adolescents are to be found in educational loss, poorer nutrition, increased exposure to intrafamiliar violence, rising incidence of mental health disorders and lack of physical activity rather than in the clinical consequences of Covid-19 infection (4-8). Inequality in education and health will increase dramatically as consequences are inevitably greater for vulnerable children due to social, material and educational poverty, disability and chronic diseases, special educational needs, and lack of access to distance learning technologies (1). The risk of dangerous habits, such as increasing...
Munro APS & Faust SL, in their viewpoint (1) quite correctly build on the evidence of low risk of contagion and rare complications of Covid-19 infection among children to call for reopening of schools. There are, however, several other good reasons to be considered.
First, as all international agencies have highlighted, prolonged closure yields serious consequences for all children and particularly for those already living in difficult circumstances, such as extreme poverty, disability, or violent environments (2,3). UNESCO estimates that at least 177 countries have instituted school closures at national level and several other countries have established closings at regional or local level (4). With over 90% of students worldwide (more than 1.5 billion young people) currently out of the educational context, it is clear that the greatest threats from Covid-19 to children and adolescents are to be found in educational loss, poorer nutrition, increased exposure to intrafamiliar violence, rising incidence of mental health disorders and lack of physical activity rather than in the clinical consequences of Covid-19 infection (4-8). Inequality in education and health will increase dramatically as consequences are inevitably greater for vulnerable children due to social, material and educational poverty, disability and chronic diseases, special educational needs, and lack of access to distance learning technologies (1). The risk of dangerous habits, such as increasing screen time and unhealthy feeding will also increase.
In Italy. 9,040,000 children and youngsters and over one million children from nursery schools and early childhood education services have been forced out of schools. Among these, 42% live in overcrowded homes, 12% in poverty, 7% in domestic environments at greater risk of abuse (9).
Second, irrespective of the magnitude of the estimates - scattered across a wide range of variability - of the contribution of school closure to reduced attack rates of the infection, they cannot be simply converted in corresponding risk of increased infection attack rates consequent to school reopening, since schools and preschool services should be not be reopened just as they were before, but following a series of safety requisites regarding teachers, accompanying caregivers, school environment and children themselves.
Third, the risk of school reopening should be measured against the risk of uncontrolled child socialization which will occur anyway, particularly when parents go back to work after lockdown and children are left with grandparents, neighbors or simply remain alone.
Finally, schools and school life represent not only a pillar of community development but also an important part of community identity. The Covid-19 pandemia will cause directly and indirectly a dramatic burden of disease and an economic catastrophe for many countries. A sensible, gradual but prompt reopening of preschool and school activities will not only reduce the risk of a dramatic crisis in child rights (2) but also contribute to restore hope in our communities.
The multidimensional adverse consequences for children of the Covid-19 pandemia have been highlighted at global level by international agencies, but they do not seem to be taken in adequate consideration at country level. Based on global knowledge about the features of the Covid-19 infection and on local epidemiological data, guidelines should be prepared for school reopening at country and local level, with a more holistic perspective of families’ and children’s needs.
A different balance must be found between the risk of increasing the number of Covid-19 cases and causing serious prejudice to children's rights.
References
1. Munro APS, Faust SN Children are not COVID-19 super spreaders: time to go back to school. Archives of Disease in Childhood Published Online First: 05 May 2020. doi: 10.1136/archdischild-2020-319474
5. Rosenthal DM, Ucci M, Heys M, Hayward A, Lakhanpaul M. Impacts of Covid- 19 on vulnerable children in temporary accommodation in the UK. Lancet Public Health 2020 March 31 https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(20)30080-3/fulltext
6. Van Lancker W, Parolin Z. Covid-19, school closures, and child poverty: a social crisis in the making. Lancet Public Health 2020 Apr 7 https://doi.org/10.1016/S2468-2667(20)30084-0
7. Green P. Risks to children and young people during Covid-19 pandemic. BMJ 2020;369:m1669 doi: 10.1136/bmj.m1669 (Published 28 April 2020)
Munro and Faust call for children to return to school despite the outstanding clinical and epidemiological questions outlined in their Viewpoint “Children are not COVID-19 super spreaders: time to go back to school”[1]. We think that their core argument – that children are minimally infected with SARS-CoV2, that they spread it less than adults, and that even children with comorbidities are relatively spared the most serious effects of COVID-19 – can be augmented with the question “is it ethical to confine children to the home for the protection of the elderly?”.
In England, 11 COVID-19 deaths were reported in 0-19 year olds up to 5 May 2020[2]. For the same period in Germany this number is three[3], and in France five[4]. During that time, the Global Burden of Disease study estimates that in each of those countries, over a thousand 0-19 year olds died from all-causes, including several hundred from road traffic injury and tens from pneumonia[5].
We do not keep children at home to protect them from these causes of death, so why are we doing this for COVID-19? We think the public, especially parents, need to understand that this is being done mainly for the benefit of adults (and especially the elderly and other vulnerable groups). This is a societal choice with immediate and potentially life-long consequences which needs careful evaluation of risks and benefits. While scientific evaluation takes place and will take time, the communication of our decision clea...
Munro and Faust call for children to return to school despite the outstanding clinical and epidemiological questions outlined in their Viewpoint “Children are not COVID-19 super spreaders: time to go back to school”[1]. We think that their core argument – that children are minimally infected with SARS-CoV2, that they spread it less than adults, and that even children with comorbidities are relatively spared the most serious effects of COVID-19 – can be augmented with the question “is it ethical to confine children to the home for the protection of the elderly?”.
In England, 11 COVID-19 deaths were reported in 0-19 year olds up to 5 May 2020[2]. For the same period in Germany this number is three[3], and in France five[4]. During that time, the Global Burden of Disease study estimates that in each of those countries, over a thousand 0-19 year olds died from all-causes, including several hundred from road traffic injury and tens from pneumonia[5].
We do not keep children at home to protect them from these causes of death, so why are we doing this for COVID-19? We think the public, especially parents, need to understand that this is being done mainly for the benefit of adults (and especially the elderly and other vulnerable groups). This is a societal choice with immediate and potentially life-long consequences which needs careful evaluation of risks and benefits. While scientific evaluation takes place and will take time, the communication of our decision clearly to the public is required now. The ethics of our choices relating to children need to be understood and debated immediately.
References
1 Munro APS, Faust SN. Children are not COVID-19 super spreaders: time to go back to school. Arch Dis Child Published Online First: 5 May 2020. doi:10.1136/archdischild-2020-319474
The question of the safety of ibuprofen in lower respiratory tract infection(LRTI)(1) should be part of a bigger question. That question is the issue of the safety of ibuprofen in a child who is at risk of dehydration. A febrile child with LRTI is at risk of dehydration because of increased insensible fluid loss via the skin. Furthermore, in the presence of LRTI-related tachypnoea, there will be increased insensible fluid loss via the upper respiratory tract . These fluid losses are compounded when the child is too ill to maintain a good oral fluid intake.
In volume depleted states, such as the scenario depicted above, vasodilatory prostaglandins maintain adequate renal blood flow(RBF) and adequate glomerular filtration rate(GFR)(2). Nonsteroidal anti inflammatory drugs(NSAIDs) undermine those compensatory mechanisms by inhibiting prostaglandin synthesis(2). The consequence is the onset of NSAID-related acute kidney injury(AKI), as postulated by Misurac et al(3). These investigators postulated that NSAID-related inhibition of prostaglandin synthesis was the underlying cause of AKI in 21 of their 27 cases of NSAID-related AKI. In the remaining 6 children with AKI, acute interstitial nephritis(also attributable to NSAIDs) was the underlying cause.. Fifteen of the 20 children for whom dosing data were available took NSAID doses in the recommended range. Ibuprofen was the culprit NSAID in 67% of cases. Misurac et al also identified 54 other cases...
The question of the safety of ibuprofen in lower respiratory tract infection(LRTI)(1) should be part of a bigger question. That question is the issue of the safety of ibuprofen in a child who is at risk of dehydration. A febrile child with LRTI is at risk of dehydration because of increased insensible fluid loss via the skin. Furthermore, in the presence of LRTI-related tachypnoea, there will be increased insensible fluid loss via the upper respiratory tract . These fluid losses are compounded when the child is too ill to maintain a good oral fluid intake.
In volume depleted states, such as the scenario depicted above, vasodilatory prostaglandins maintain adequate renal blood flow(RBF) and adequate glomerular filtration rate(GFR)(2). Nonsteroidal anti inflammatory drugs(NSAIDs) undermine those compensatory mechanisms by inhibiting prostaglandin synthesis(2). The consequence is the onset of NSAID-related acute kidney injury(AKI), as postulated by Misurac et al(3). These investigators postulated that NSAID-related inhibition of prostaglandin synthesis was the underlying cause of AKI in 21 of their 27 cases of NSAID-related AKI. In the remaining 6 children with AKI, acute interstitial nephritis(also attributable to NSAIDs) was the underlying cause.. Fifteen of the 20 children for whom dosing data were available took NSAID doses in the recommended range. Ibuprofen was the culprit NSAID in 67% of cases. Misurac et al also identified 54 other cases of NSAID-related AKI in the medical literature during the period 1993 to 2009. Sixty percent of 50 cases for whom dosing data were available took the recommended does of NSAID. Fifty-three percent of the 54 cases were documented as having experienced reduced fluid intake before admission. Ibuprofen was the culprit NSAID in 20 of the 54 cases.
Comment
In the presence of LRTI-related dehydration ibuprofen has the potential to precipitate AKI as a result of NSAID-related inhibition of prostaglandin synthesis.
I have no funding and no conflict of interest
References
(1) Skehin K., Thompson A., Moriarty P
Is use of ibuprofen safe in children with signs and symptoms of lower respiratory tract infection?
Arch Dis Child 2019 Epub ahead of print
(2) Kim G-H
Renal effects of prostaglandins and cyclooxygenase-2 inhibitors
Electrolyte & Bood Disorders 2008;6:35-41
(3)Misurac JM., Knoderer CA., Leiser D et al
Nonsteroidal anti-inflammatory drugs are an important cause of acute kidney injury in children
J Pediatr 2013;162:1153-1159
Infant vitamin D supplementation prevents not just rickets but also hypocalcaemic seizures and cardiomyopathy (CMP). The BPSU survey (1) captures rickets incidence which, we feel compelled to highlight, represents only the tip of the iceberg of widespread vitamin D deficiency (VDD) in the population.
In the UK, child surveillance checks are led by general practitioners (GPs). Most GPs do not receive postgraduate paediatric training and have inadequate undergraduate paediatric exposure, as acknowledged by the RCPCH president: “by any stretch of the imagination, GP training in the UK in paediatrics is woefully inadequate” (2). Recognising rickets requires paediatric experience as exemplified by recent cases of VDD induced CMP- one child’s death was preceded by multiple unfruitful visits to GPs and casualty (3). As the BPSU survey reached out only to paediatricians and not GPs, the extent of underreporting and under diagnosis is likely huge, limiting comparison with countries where paediatricians oversee primary care. The conclusion that rickets incidence in the UK is lower than expected downplays the extent of the underlying public health crisis, particularly when a significant number of cases were excluded [table 2 of (1)]. The true disease burden is unravelled when family members of affected children are investigated (3).
Similar to previous studies, rickets incidence here is 90 to 166 fold higher in Asian and Black children compared to wh...
Infant vitamin D supplementation prevents not just rickets but also hypocalcaemic seizures and cardiomyopathy (CMP). The BPSU survey (1) captures rickets incidence which, we feel compelled to highlight, represents only the tip of the iceberg of widespread vitamin D deficiency (VDD) in the population.
In the UK, child surveillance checks are led by general practitioners (GPs). Most GPs do not receive postgraduate paediatric training and have inadequate undergraduate paediatric exposure, as acknowledged by the RCPCH president: “by any stretch of the imagination, GP training in the UK in paediatrics is woefully inadequate” (2). Recognising rickets requires paediatric experience as exemplified by recent cases of VDD induced CMP- one child’s death was preceded by multiple unfruitful visits to GPs and casualty (3). As the BPSU survey reached out only to paediatricians and not GPs, the extent of underreporting and under diagnosis is likely huge, limiting comparison with countries where paediatricians oversee primary care. The conclusion that rickets incidence in the UK is lower than expected downplays the extent of the underlying public health crisis, particularly when a significant number of cases were excluded [table 2 of (1)]. The true disease burden is unravelled when family members of affected children are investigated (3).
Similar to previous studies, rickets incidence here is 90 to 166 fold higher in Asian and Black children compared to white. As the proportion of ethnic minority in the UK continues to rise (14% in 2011 census) those at highest risk of VDD are failed most by inadequate prevention strategies (4).
Shockingly, 77% of reported cases were not on the Department of Health recommended vitamin D supplements demonstrating lack of policy implementation. Whilst we agree with the author’s recommendations on supplementation, vitamin D fortification of flour as a more cost-effective long term strategy should be seriously considered (5).
References:
1. Julies P, Lynn RM, Pall K, Leoni M, Calder A, Mughal Z, et al. Nutritional rickets under 16 years : UK surveillance results. Arch Dis Child. 2020;
2. Modi N, Simon C. Child health care: Adequate training for all UK GPs is long overdue. Br J Gen Pract. 2016;66(646):228–9.
3. Uday S, Fratzl-Zelman N, Roschger P, Klaushofer K, Chikermane A, Saraff V, et al. Cardiac, bone and growth plate manifestations in hypocalcemic infants: revealing the hidden body of the vitamin D deficiency iceberg. BMC Pediatr. 2018 Dec;18(1):183.
4. Uday S, Högler W. Prevention of rickets and osteomalacia in the UK: political action overdue. Arch Dis Child. 2018;103(9):901–6.
5. Aguiar M, Andronis L, Pallan M, Högler W, Frew E. The economic case for prevention of population vitamin D deficiency: a modelling study using data from England and Wales. Eur J Clin Nutr. 2019; DOI:10.1038/s41430-019-0486-x
We write in response to the article "Use of oral corticosteroids in the treatment of alopecia areata" by BJ Cowley and J Dong, published in January's edition of the journal.(1)
In this article, the authors present a summary of their literature search, concluding that oral corticosteroid pulse therapy may be a safe and effective treatment for sufferers of alopecia areata (AA). The authors highlight the risk of avascular necrosis of the hip with the use of corticosteroids, despite none of their cited studies reporting on this complication specifically.
We would argue that iatrogenic adrenal suppression (AS) secondary to exogenous corticosteroid administration is also a noteworthy risk in these patients. Symptomatic AS has been well documented in the asthmatic population receiving daily inhaled corticosteroids, occasionally resulting in adrenal crisis and even sadly death. Whilst there is a good level of awareness of AS amongst some colleagues using high doses of daily steroids, for example in the induction phases of leukaemia treatment, AS is not confined to these children and is as pertinent to those receiving pulsed steroids for AA(2,3).
In our centre we have had personal experience of looking after a child who required intubation and ventilation when they developed a viral illness and presented with hypotension and hypoglycaemia. They had received intralesional steroids to treat AA, which had caused severe adrenal sup...
We write in response to the article "Use of oral corticosteroids in the treatment of alopecia areata" by BJ Cowley and J Dong, published in January's edition of the journal.(1)
In this article, the authors present a summary of their literature search, concluding that oral corticosteroid pulse therapy may be a safe and effective treatment for sufferers of alopecia areata (AA). The authors highlight the risk of avascular necrosis of the hip with the use of corticosteroids, despite none of their cited studies reporting on this complication specifically.
We would argue that iatrogenic adrenal suppression (AS) secondary to exogenous corticosteroid administration is also a noteworthy risk in these patients. Symptomatic AS has been well documented in the asthmatic population receiving daily inhaled corticosteroids, occasionally resulting in adrenal crisis and even sadly death. Whilst there is a good level of awareness of AS amongst some colleagues using high doses of daily steroids, for example in the induction phases of leukaemia treatment, AS is not confined to these children and is as pertinent to those receiving pulsed steroids for AA(2,3).
In our centre we have had personal experience of looking after a child who required intubation and ventilation when they developed a viral illness and presented with hypotension and hypoglycaemia. They had received intralesional steroids to treat AA, which had caused severe adrenal suppression. This took a year to fully recover as evidenced by serial synacthen tests. They had no evidence of any primary adrenal pathology.
We therefore feel strongly that in this education-focused article, it is remiss not to highlight adrenal suppression as a key risk with any corticosteroid regimen.
Dr Elizabeth M Bayman, Dr Louise E Bath, Prof Amanda J Drake
1. Cowley BJ, Dong J. Use of oral corticosteroids in the treatment of alopecia areata. Archives of Disease in Childhood 2020;105:96-98.
2. Goldbloom EB, Mokashi A, Cummings EA, et al. Symptomatic adrenal suppression among children in Canada. Arch Dis Child. 2017 Apr;102(4):340-345.
3. Bayman EM, Drake AJ. Adrenal suppression, still a problem after all these years. Arch Dis Child. 2017 Apr;102(4):338-339.
I read with interest your recent publication “Language in 2-year-old children born preterm and term: a cohort study) in the Archives of Disease in Childhood. I have made certain observations, and would welcome your views on them.
I notice (Figure 1) that you screened 557 preterm infants for eligibility. Ninety three of these were excluded as they were deemed unsuitable by medical staff and another hundred and seventeen were excluded for other reasons. As those numbers are quite substantial, I am curious to know what those factors were, and think that some details on those factors will further enhance the quality of the paper.
Your preterm cohort is defined as <30 weeks gestation. The current evidence shows that mortality and morbidity in preterm babies is associated with degree of prematurity. Therefore, I am wondering that what was the distribution of gestational age in the group and was there any further subgroup analysis attempted.
You mentioned family history having an impact on the likelihood of language delay in the introduction. However, I note that this was not included in list of factors explored. I wonder if there was any particular reason to do so.
I look forward to hearing from you, and would like to thank you in anticipation for your time.
Many thanks,
Dr Anna Howells
Paediatric SPR
Community Paediatrics, Bromley
We enjoyed reading the study by Jaquet-Pilloud et al. 1 examining the role of nebulised 3% hypertonic saline (HS) and bronchiolitis. We thank the authors for this excellent pragmatic non-blinded, randomised controlled trial. Their conclusions support the UK evidence from the SABRE study 2 and their systematic review3 which provides evidence of the futility of adding hypertonic saline to the management of bronchiolitis when compared to standard care alone with length of stay (LOS) or ready for discharge as the primary outcome. The article was well written and easy to follow. The study examined 121 infants with bronchiolitis recruited over three years from one tertiary centre in Switzerland. We felt it illustrated the very important problem of underpowered studies concluding no differences between two treatment regimens. The authors used the Korppi et al 3 study to assume that the mean LOS for infants admitted to hospital with bronchiolitis was 5 days [120 hours] with a standard deviation of 1.2 days [28.8 hours]. Reduction in hospital stay by 1 day was considered clinically significant and based on this a minimum sample size of 120 (with 60 in each group) was arrived. However the data from this paper by Jaquet-Pilloud et al show that the mean LOS was 47 hours (± 8.5) for nebulised hypertonic saline group and 50.4 hours (±11) for standard care group. The LOS at the authors’ hospital was less than half of the assumption used for their power calculation....
We enjoyed reading the study by Jaquet-Pilloud et al. 1 examining the role of nebulised 3% hypertonic saline (HS) and bronchiolitis. We thank the authors for this excellent pragmatic non-blinded, randomised controlled trial. Their conclusions support the UK evidence from the SABRE study 2 and their systematic review3 which provides evidence of the futility of adding hypertonic saline to the management of bronchiolitis when compared to standard care alone with length of stay (LOS) or ready for discharge as the primary outcome. The article was well written and easy to follow. The study examined 121 infants with bronchiolitis recruited over three years from one tertiary centre in Switzerland. We felt it illustrated the very important problem of underpowered studies concluding no differences between two treatment regimens. The authors used the Korppi et al 3 study to assume that the mean LOS for infants admitted to hospital with bronchiolitis was 5 days [120 hours] with a standard deviation of 1.2 days [28.8 hours]. Reduction in hospital stay by 1 day was considered clinically significant and based on this a minimum sample size of 120 (with 60 in each group) was arrived. However the data from this paper by Jaquet-Pilloud et al show that the mean LOS was 47 hours (± 8.5) for nebulised hypertonic saline group and 50.4 hours (±11) for standard care group. The LOS at the authors’ hospital was less than half of the assumption used for their power calculation. Our calculation suggests that based on authors LOS, the minimum sample should be at least 240 subjects. This calculation was similar to the numbers recruited in the SABRE study which used the UK hospital episode statistics that suggested that the average (mean (SD)) time to discharge was 72 (32) hours to power their study and with three years of recruitment and a total of 317 infants in this study with 158 infants randomised to HS and 159 to standard care. There was no difference between the two arms in time to being declared fit for discharge. They showed the median (not mean in this paper) time to being declared fit for discharge was 76 hours from admission in each group, and the time to actual discharge was 89 hours in each group. Essentially Jaquet-Pilloud et al needed twice as many subjects to be sure that there was no type 2 error and to be confident about the accuracy of their conclusions.
Yours sincerely
Dr Muthukumar Sakthivel, Dr Dure Yasrab, Dr Kevin Enright and Professor Colin Powell
Pediatric Emergency Department Sidra Medicine, Doha, Qatar
We read with interest Dr. Smee et al.’s article on surfactant administration via laryngeal mask (LMA) in infants with respiratory distress syndrome: an intriguing topic, suggesting a minimally invasive approach to ensure a well-established therapy.
Show MoreThe authors stated that “use of LMA to administer surfactant is feasible in infants ≥ 1200g, reducing the need for intubation and mechanical ventilation”. (1) Despite a recent meta-analysis showing that this approach may have some advantages on short term outcomes, (i.e. reduction in need for intubation and mechanical ventilation), available evidence was based on small, poor-quality studies. (2)
In addition, there are many unanswered questions on the application of this approach in neonates. It is not known which supraglottic airway device (SAD) may be best suited (there are at least 7 different types of commercially available size-1 SADs), the characteristics of the cuff (inflatable or not-inflatable) and the most appropriate size, (3,4) whether a catheter inside the mask should be used and if yes, where the catheter’s tip should be positioned (proximally or distally), under vision or blindly. There is uncertainty on whether the patient needs mild sedation, general or topical anesthesia, or nothing at all, and around the best mode to support respiratory efforts and potential complications (i.e. hypoxia or bradycardia) during the procedure. (1)
The authors also reported that “LMAs to fit the more immature infan...
e-Letter
Low Prevalence of Kingella kingae Infections in UK Children
Pablo Yagupsky, MD
Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel
Corresponding Author: Pablo Yagupsky, Clinical Microbiology Laboratory, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel 84101. Phone number: (972) 506264359. Fax number: (972) 86403541. e-mail: PYagupsky@gmail.com
Show MoreDear Editor:
In a recent article, Abeywickrema et al. summarized 10 years of pediatric joint and bone infections in Oxford, and concluded that Staphylococcus aureus was the most common etiology [1]. Although this concept was widely accepted in the past, the increasing use of sensitive nucleic acid amplification tests has demonstrated that Kingella kingae is the leading agent of skeletal system infections in the 6-48 month-old population, causing up to 88% of the cases in this age group [2]. Abeywickrema et al., however, isolated the bacterium in only 3 of the 74 (4%) patients in whom the etiology could be determined [1]. Kingella kingae is notoriously fastidious and the traditional culture methods and microscopy employed by the researchers are usually unable to detect its presence in joint and bone exudates [3]. Invasive K. kingae infections other than endocarditis are characterized by a mild local and systemic inflammation: fev...
Since the introduction of the national delay phase response to Covid-19 Coronavirus in the republic of Ireland on March 12th and subsequent advise to stay at home from March 27th, essential paediatric cardiac services have had to continue in a limited capacity.
In that time, our national tertiary referral centre has seen 428 children in the out-patient's setting, 223 on the cardiac day ward, and performed an intervention (cardiac surgery or cardiac catheterization) in 140 cases. This includes 41 cardiac by-pass cases, 22 non-bypass cases, 49 interventional cardiac catheterization cases and 6 hybrid procedures involving both the cardiac surgery and cardiac catheterization teams.
Of the 49 patients screened pre-operatively, not one positive (and asymptomatic) case was identified.
Adhering to government advice on social distancing and appropriate PPE where indicated, not a single member of the extended medical team has been known to cntract Covid-19 Coronavirus from contact with patients or their families in this time.
This anecdotal case experience from one institution supports the proposal to allow children to return to school regardless of comorbidities, in recognition of the considerable long-term educational and social harm that exclusion would result in.
Munro APS & Faust SL, in their viewpoint (1) quite correctly build on the evidence of low risk of contagion and rare complications of Covid-19 infection among children to call for reopening of schools. There are, however, several other good reasons to be considered.
First, as all international agencies have highlighted, prolonged closure yields serious consequences for all children and particularly for those already living in difficult circumstances, such as extreme poverty, disability, or violent environments (2,3). UNESCO estimates that at least 177 countries have instituted school closures at national level and several other countries have established closings at regional or local level (4). With over 90% of students worldwide (more than 1.5 billion young people) currently out of the educational context, it is clear that the greatest threats from Covid-19 to children and adolescents are to be found in educational loss, poorer nutrition, increased exposure to intrafamiliar violence, rising incidence of mental health disorders and lack of physical activity rather than in the clinical consequences of Covid-19 infection (4-8). Inequality in education and health will increase dramatically as consequences are inevitably greater for vulnerable children due to social, material and educational poverty, disability and chronic diseases, special educational needs, and lack of access to distance learning technologies (1). The risk of dangerous habits, such as increasing...
Show MoreMunro and Faust call for children to return to school despite the outstanding clinical and epidemiological questions outlined in their Viewpoint “Children are not COVID-19 super spreaders: time to go back to school”[1]. We think that their core argument – that children are minimally infected with SARS-CoV2, that they spread it less than adults, and that even children with comorbidities are relatively spared the most serious effects of COVID-19 – can be augmented with the question “is it ethical to confine children to the home for the protection of the elderly?”.
In England, 11 COVID-19 deaths were reported in 0-19 year olds up to 5 May 2020[2]. For the same period in Germany this number is three[3], and in France five[4]. During that time, the Global Burden of Disease study estimates that in each of those countries, over a thousand 0-19 year olds died from all-causes, including several hundred from road traffic injury and tens from pneumonia[5].
We do not keep children at home to protect them from these causes of death, so why are we doing this for COVID-19? We think the public, especially parents, need to understand that this is being done mainly for the benefit of adults (and especially the elderly and other vulnerable groups). This is a societal choice with immediate and potentially life-long consequences which needs careful evaluation of risks and benefits. While scientific evaluation takes place and will take time, the communication of our decision clea...
Show MoreThe question of the safety of ibuprofen in lower respiratory tract infection(LRTI)(1) should be part of a bigger question. That question is the issue of the safety of ibuprofen in a child who is at risk of dehydration. A febrile child with LRTI is at risk of dehydration because of increased insensible fluid loss via the skin. Furthermore, in the presence of LRTI-related tachypnoea, there will be increased insensible fluid loss via the upper respiratory tract . These fluid losses are compounded when the child is too ill to maintain a good oral fluid intake.
Show MoreIn volume depleted states, such as the scenario depicted above, vasodilatory prostaglandins maintain adequate renal blood flow(RBF) and adequate glomerular filtration rate(GFR)(2). Nonsteroidal anti inflammatory drugs(NSAIDs) undermine those compensatory mechanisms by inhibiting prostaglandin synthesis(2). The consequence is the onset of NSAID-related acute kidney injury(AKI), as postulated by Misurac et al(3). These investigators postulated that NSAID-related inhibition of prostaglandin synthesis was the underlying cause of AKI in 21 of their 27 cases of NSAID-related AKI. In the remaining 6 children with AKI, acute interstitial nephritis(also attributable to NSAIDs) was the underlying cause.. Fifteen of the 20 children for whom dosing data were available took NSAID doses in the recommended range. Ibuprofen was the culprit NSAID in 67% of cases. Misurac et al also identified 54 other cases...
Dear Editor
Infant vitamin D supplementation prevents not just rickets but also hypocalcaemic seizures and cardiomyopathy (CMP). The BPSU survey (1) captures rickets incidence which, we feel compelled to highlight, represents only the tip of the iceberg of widespread vitamin D deficiency (VDD) in the population.
In the UK, child surveillance checks are led by general practitioners (GPs). Most GPs do not receive postgraduate paediatric training and have inadequate undergraduate paediatric exposure, as acknowledged by the RCPCH president: “by any stretch of the imagination, GP training in the UK in paediatrics is woefully inadequate” (2). Recognising rickets requires paediatric experience as exemplified by recent cases of VDD induced CMP- one child’s death was preceded by multiple unfruitful visits to GPs and casualty (3). As the BPSU survey reached out only to paediatricians and not GPs, the extent of underreporting and under diagnosis is likely huge, limiting comparison with countries where paediatricians oversee primary care. The conclusion that rickets incidence in the UK is lower than expected downplays the extent of the underlying public health crisis, particularly when a significant number of cases were excluded [table 2 of (1)]. The true disease burden is unravelled when family members of affected children are investigated (3).
Similar to previous studies, rickets incidence here is 90 to 166 fold higher in Asian and Black children compared to wh...
Show MoreDear editor
We write in response to the article "Use of oral corticosteroids in the treatment of alopecia areata" by BJ Cowley and J Dong, published in January's edition of the journal.(1)
In this article, the authors present a summary of their literature search, concluding that oral corticosteroid pulse therapy may be a safe and effective treatment for sufferers of alopecia areata (AA). The authors highlight the risk of avascular necrosis of the hip with the use of corticosteroids, despite none of their cited studies reporting on this complication specifically.
We would argue that iatrogenic adrenal suppression (AS) secondary to exogenous corticosteroid administration is also a noteworthy risk in these patients. Symptomatic AS has been well documented in the asthmatic population receiving daily inhaled corticosteroids, occasionally resulting in adrenal crisis and even sadly death. Whilst there is a good level of awareness of AS amongst some colleagues using high doses of daily steroids, for example in the induction phases of leukaemia treatment, AS is not confined to these children and is as pertinent to those receiving pulsed steroids for AA(2,3).
In our centre we have had personal experience of looking after a child who required intubation and ventilation when they developed a viral illness and presented with hypotension and hypoglycaemia. They had received intralesional steroids to treat AA, which had caused severe adrenal sup...
Show MoreDear Sanchez et al,
I read with interest your recent publication “Language in 2-year-old children born preterm and term: a cohort study) in the Archives of Disease in Childhood. I have made certain observations, and would welcome your views on them.
I notice (Figure 1) that you screened 557 preterm infants for eligibility. Ninety three of these were excluded as they were deemed unsuitable by medical staff and another hundred and seventeen were excluded for other reasons. As those numbers are quite substantial, I am curious to know what those factors were, and think that some details on those factors will further enhance the quality of the paper.
Your preterm cohort is defined as <30 weeks gestation. The current evidence shows that mortality and morbidity in preterm babies is associated with degree of prematurity. Therefore, I am wondering that what was the distribution of gestational age in the group and was there any further subgroup analysis attempted.
You mentioned family history having an impact on the likelihood of language delay in the introduction. However, I note that this was not included in list of factors explored. I wonder if there was any particular reason to do so.
I look forward to hearing from you, and would like to thank you in anticipation for your time.
Many thanks,
Dr Anna Howells
Paediatric SPR
Community Paediatrics, Bromley
Dear Editor
We enjoyed reading the study by Jaquet-Pilloud et al. 1 examining the role of nebulised 3% hypertonic saline (HS) and bronchiolitis. We thank the authors for this excellent pragmatic non-blinded, randomised controlled trial. Their conclusions support the UK evidence from the SABRE study 2 and their systematic review3 which provides evidence of the futility of adding hypertonic saline to the management of bronchiolitis when compared to standard care alone with length of stay (LOS) or ready for discharge as the primary outcome. The article was well written and easy to follow. The study examined 121 infants with bronchiolitis recruited over three years from one tertiary centre in Switzerland. We felt it illustrated the very important problem of underpowered studies concluding no differences between two treatment regimens. The authors used the Korppi et al 3 study to assume that the mean LOS for infants admitted to hospital with bronchiolitis was 5 days [120 hours] with a standard deviation of 1.2 days [28.8 hours]. Reduction in hospital stay by 1 day was considered clinically significant and based on this a minimum sample size of 120 (with 60 in each group) was arrived. However the data from this paper by Jaquet-Pilloud et al show that the mean LOS was 47 hours (± 8.5) for nebulised hypertonic saline group and 50.4 hours (±11) for standard care group. The LOS at the authors’ hospital was less than half of the assumption used for their power calculation....
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