1577 e-Letters

  • Children are being kept at home to protect the elderly from COVID-19

    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...

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  • Other mechanisms for coeliac disease-related hypocalcaemia

    For the sake of completeness, the account of underlying causes of hypocalcaemia(Table 2)(1) should also include hypoparathyroidism-related hypocalcaemia attributable to magnesium deficiency(2), and coeliac disease-related hypocalcaemia which is not attributable to vitamin D deficiency(3). The role of hypoparathyroidism was documented in a 12 year old patient in whom hypoparathyroidism was thought to be attributable to inhibition of parathyroid hormone(PTH) release as a result of coeliac disease(CD)-related magnesium malabsorption. This patient had been admitted with hypocalcaemia, hypomagnesemia, hyperphosphataemia and subnormal serum vitamin D level of 8 mg/ml(normal 20-45 ng/ml). The plasma parathyroid hormone(PTH) level(14.6 pg/ml; normal > 12 pg/ml) was only minimally elevated, which was inappropriate in relation to the plasma calcium level of 5.1 mg/dl. Sm,all bowel biopsy showed moderate villous atrophy. Despite treatment with gluten free diet(GFD), and replacement therapy comprising vitamin D, calcium, magnesium , and aluminium hydroxide as a phosphate binder, calcium and magnesium levels were initially persistently low and phosphorus levels were persistently high. Furthermore, serum PTH levels also subsequently became undetectable. It was only after magnesium levels and calcium levels rose that phosphorus levels and serum PTH levels normalised. The authors hypothesised that CD had been the underlying cause of both the hypocalcaemia and...

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  • Cowpox inncoluaiton scare 1806

    I welcome this important historical paper emphasising the continued extreme importance of immunisation over more than 2 centuries in effectively preventing avoidable death and disability in children .
    I was very surprised though, that the authors omitted a short paper published in the ADC in 2004 which related an 1806 inoculation scare in Northampton UK,. Northampton General Infirmary commenced giving free cowpox inoculations to the poor from 1January 11th 1804. In January 1806 there was an inoculation scare that led to a marked drop in public confidence after rumours of the death of a child Peter Bell. This was thoroughly investigated by the Infirmary Committee and in the Northampton Mercury of 10th January 1806 his parents had published a signed declaration that their son's death was nothing at all to do with the cowpox inoculation.
    Public confidence was then restored

    Williams A.N, A Vaccine Scare in 19th Century Northampton Arch Dis Child. 2005 Nov;90(11):1204.

  • Preventing infant regulation problems: considering the roles of biology and parenting

    Infant sleeping, crying and feeding problems can be hugely concerning for parents. As Wolke points out,(1) a growing body of evidence points to a range of poor longer term outcomes for infants who experience persistent, severe, regulatory difficulties. Olsen and colleagues’ study(2) is important because it aims to help our understanding of the early factors that predict persistent regulatory difficulties. If we can identify these early risk factors, perhaps we can better focus our efforts to prevent these difficulties from arising.

    There have been several attempts to prevent infant sleeping and crying difficulties via parent education and support programs. Randomized controlled trials of these programs have reported small increases in infant sleep duration, increased likelihood of ‘sleeping through the night’,(3–5) reduced parent depressive symptoms, and less doubt about parenting ability at bedtime.(6) Parent education programs may modestly reduce infant sleep difficulties. Whether these infants are then less likely to develop complex regulatory problems that precede poor childhood outcomes, remains to be tested.

    We agree with Wolke’s assertion that ‘there is a major need to educate parents on how to support infants in regulatory adaptation.’ Parenting practices such as having a consistent bedtime routine, and encouraging independent settling, have been shown to improve infant sleep.(7) However, we must consider that some infants’ sleep difficulties may have...

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  • Response to Professor Cook et al.'s letter

    Dear Editor,
    We thank Professor Cook et al. for their letter in response to our Archimedes paper. We agree that waveform capnography may have benefit in earlier detection of oesophageal intubation or unplanned extubations in neonates, as has been assumed in adults. However, this assumption will require further study. Following an UK expert panel meeting, we are looking forward to investigating the use of waveform capnography monitoring in neonates.
    As previously discussed in correspondence with Dr Whitaker, there are two pertinent questions to answer here for the neonatal population:
    1) In neonates (P), does the addition of waveform capnography (I) compared to current methods of detection (colourimetric capnography, ventilator measurements, oxygen saturations and clinical examination) (C) provide an advantage in earlier detection of oesophageal intubation or unplanned extubation (O)?
    2) Does the displayed numerical value in waveform capnography correlate with PaCO2 reliably enough to guide ventilator changes?
    In our review, we specifically sought to address the second question. Those familiar with contemporary neonatal practice will know that many NICUs use transcutaneous capnography. Question 2 has a particular pertinence in neonates as their physiology is different from the adult and even paediatric population. Neonates are particularly prone to rapid changes in PaCO2, due to their changing lung compliance. Due to their lack of cerebral auto...

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  • The risk of ibuprofen-related acute kidney injury is just as important

    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...

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  • Response letter to Nutritional rickets under 16 years: UK surveillance results

    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...

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  • Latrogenic adrenal suppression, a risk not be to ignored

    Dear 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...

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  • Observations

    Dear 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

  • Letter to Editor Nebulised hypertonic saline in moderate-to-severe bronchiolitis: a randomised clinical trial. Raphaelle Jaquet-Pilloud, Marie-Elise Verga, Michel Russo, Mario Gehri, Jean-Yves Pauchard

    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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