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
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...
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 the hypomagnesemia. The latter , in turn, had inhibited PTH release, thereby aggravating the hypocalcaemia. Ultimately, rigorous adherence to GFD led to normalisation of serum magnesium and, hence, normalisation of serum PTH, thereby contributing to GFD-related normalisation of serum calcium levels.(2).
In the adult context coeliac disease(CD) can also manifest as isolated hypocalcaemia in the presence of normal serum magnesium, normal serum phosphorus, normal vitamin D levels, and appropriately elevated serum PTH. This scenario was reported in a 36 year old woman in whom the clinicians hypothesised that hypocalcaemia was solely attributable to CD-related malabsorption of calcium, independent of vitamin D status(3). A similar scenario would be plausible in paediatrics , although hitherto unreported in that context.
I have no funding and no conflict of interest.
References
(1) Nadar R., Shaw N
Investigation and management of hypocalcemia
Arch Dis Child 2020;105:399-405
(2)Yerushalmi B., Lev-Tzion R., Loewenthal N
Refractory hypoparathyroidism in a child with celiac disease
IMAJ 2016;18:58-60
(3)Rickels MR., Mandel SJ
Celiac disease manifesting as isolated hypocalcemia
Endocr Parct 2004;10:203-207
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
Reference
Williams A.N, A Vaccine Scare in 19th Century Northampton Arch Dis Child. 2005 Nov;90(11):1204.
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...
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 less to do with parenting practices, and more to do with prenatal exposure to stress and other adversities. For these infants, sleep may not be easily improved with typical infant sleep interventions.
Prenatal maternal depression, anxiety, and stress are associated with increased risk for poorer infant health, greater infant stress reactivity and increased risk for preterm birth and low birth weight - factors that are known to contribute to increased regulatory problems.(8,9) Epigenetic influences on NR3C1 gene expression have been suggested to explain the association between heightened stress during pregnancy and later infant neuroendocrine function, behavior regulation and temperament.(10–12) Other research indicates that neurodevelopmental vulnerabilities and prenatal exposure to stress, better predict persistent regulatory difficulties than parenting style.(2,9,13)
While there is strong evidence that parenting practices influence infant sleep and crying behaviors,(7) emerging evidence seems to suggest that prenatal biological factors may also play a critical role. We do not yet know whether the effect of prenatal stress and adversity on later infant sleep can be changed via improved/altered parenting practices. Perhaps this explains why a small proportion of parents who report infant regulation problems insist that nothing helps their infant to sleep better. Instead of asking these parents to keep trying/try harder, it may be more beneficial to consider what other supports can help these families cope.
Further research is necessary to understand how nature and nurture intersect to influence the development of infant regulation. Findings will ultimately inform development of targeted, early prevention strategies that might improve outcomes for all dysregulated infants and their families.
1. Wolke D. Persistence of infant crying, sleeping and feeding problems: Need for prevention. Vol. 104, Archives of Disease in Childhood. 2019. p. 1022–3.
2. Olsen AL, Ammitzbøll J, Olsen EM, Skovgaard AM. Problems of feeding, sleeping and excessive crying in infancy: A general population study. Arch Dis Child. 2019 Jul 3 ;Epub ahead.
3. St James-Roberts I, Sleep J, Morris S, Owen C, Gillham P. Use of a behavioural programme in the first 3 months to prevent infant crying and sleeping problems. J Paediatr Child Health. 2001 Jun;37(3):289–97.
4. Symon BG, Marley JE, Martin AJ, Norman ER. Effect of a consultation teaching behaviour modification on sleep performance in infants: a randomised controlled trial. Med J Aust. 2005 Mar 7;182(5):215–8.
5. Pinilla T, Birch LL. Help me make it through the night: behavioral entrainment of breast-fed infants’ sleep patterns. Pediatrics. 1993 Feb;91(2):436–44.
6. Hiscock H, Cook F, Bayer J, Le HND, Mensah F, Cann W, et al. Preventing Early Infant Sleep and Crying Problems and Postnatal Depression: A Randomized Trial. Pediatrics. 2014 Feb 1;133(2):e346-54.
7. Sadeh A, Tikotzky L, Scher A. Parenting and infant sleep. Sleep Med Rev. 2010 Apr;14(2):89–96.
8. Nazzari S, Fearon P, Rice F, Dottori N, Ciceri F, Molteni M, et al. Beyond the HPA-axis: Exploring maternal prenatal influences on birth outcomes and stress reactivity. Psychoneuroendocrinology. 2019 Mar 14;101:253–62.
9. Bilgin A, Wolke D. Development of comorbid crying, sleeping, feeding problems across infancy: Neurodevelopmental vulnerability and parenting. Early Hum Dev. 2017 Jun;109(March 2017):37–43.
10. Conradt E, Fei M, LaGasse L, Tronick E, Guerin D, Gorman D, et al. Prenatal predictors of infant self-regulation: the contributions of placental DNA methylation of NR3C1 and neuroendocrine activity. Front Behav Neurosci. 2015 May 29;9:130.
11. Glover V, O’Donnell KJ, O’Connor TG, Fisher J. Prenatal maternal stress, fetal programming, and mechanisms underlying later psychopathology—A global perspective. Dev Psychopathol. 2018 Aug 2;30(03):843–54.
12. Van den Bergh BRH, Mulder EJH, Mennes M, Glover V. Antenatal maternal anxiety and stress and the neurobehavioural development of the fetus and child: links and possible mechanisms. A review. Neurosci Biobehav Rev. 2005 Apr;29(2):237–58.
13. Cook F, Conway L, Gartland D, Giallo R, Keys E, Brown S. Profiles and Predictors of Infant Sleep Problems Across the First Year. J Dev Behav Pediatr. 2019 Sep;1.
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...
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 autoregulation, changes in PaCO2 have a direct effect on blood flow to and around the brain. Swings in PaCO2 are known to be associated with poorer long term outcomes, severe neurological complications including intraventricular haemorrhage and potentially death. Thus, whenever a measured value is presented, it is important that staff are trained to interpret the value in the clinical setting to adequately respond, re-evaluate and avoid mistakes.
Despite the PICNIC survey’s merits as a thorough and well carried out national survey, PICNIC was reported by the mainstream media in a manner which may cause undue distress amongst NICU parents. Therefore, we aimed to highlight this problem in our opening paragraph. Regrettably, media misinterpretation is not an infrequent issue.
We are surprised by the comment by Prof. Cook et al. that our review omits the study by Kugelman et al. Their 2016 study on the impact of continuous capnography in ventilated neonates is included, both in the table and as reference number 30 of our paper. This study involved a small number of infants, relied on parameters set by ETCO2 (which has been shown by other studies not to approximate well to PaCO2) and was clearly underpowered to detect differences in neurological outcomes between groups.
To conclude, we feel there may be a role for waveform capnography in neonatal practice providing that concerns about safety (interference with volume guarantee ventilation, auto-triggering of ventilators, etc.) can be alleviated through careful study. If proven effective, waveform capnography must be adopted together with a clear understanding of its benefits and limitations, as well as training for all medical and nursing staff to avoid harm and ensure maximum benefit to patients.
A Scrivens
S Zivanovic
CC Roehr
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
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 MoreFor 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...
Show MoreI 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
Reference
Williams A.N, A Vaccine Scare in 19th Century Northampton Arch Dis Child. 2005 Nov;90(11):1204.
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...
Show MoreDear Editor,
Show MoreWe 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...
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.
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...
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