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Sir,
I would like to add to the article ‘What dose of aspirin should be used in the initial treatment of Kawasaki disease?’ by Luke Guo Yang Ho and Nigel Curtis (Archives, 2017, 102, 1180-1182). Fifteen months have passed since this article concluded that low-dose aspirin is not inferior to higher doses in reducing the risk of coronary artery abnormalities in acute Kawasaki disease. Since then, it is worth considering what and if anything has changed in the field. A recent study not included in the review is a retrospective cohort study by Huang et al1 (2018), where 910 patients followed up for 2 years, which showed that there was no significant difference between 3 groups in terms of anti-inflammation or prevention of coronary artery abnormalities. This paper concluded that the role of aspirin in the treatment of the acute phase of Kawasaki disease should be questioned, as a definite benefit has not been shown. Therefore, in concordance with the conclusion of the review, this rapid response poses that current data remains unchanged with regards to the role and effects of administration of higher doses of aspirin on coronary outcome in acute Kawasaki disease. In the absence of evidence to support higher doses in prevention of coronary artery abnormalities, low-dose aspirin (3–5 mg/kg) may be the safest, most rational approach until better evidence becomes available.
There are currently three prospective randomised control trials in process to continue this inv...
Sir,
I would like to add to the article ‘What dose of aspirin should be used in the initial treatment of Kawasaki disease?’ by Luke Guo Yang Ho and Nigel Curtis (Archives, 2017, 102, 1180-1182). Fifteen months have passed since this article concluded that low-dose aspirin is not inferior to higher doses in reducing the risk of coronary artery abnormalities in acute Kawasaki disease. Since then, it is worth considering what and if anything has changed in the field. A recent study not included in the review is a retrospective cohort study by Huang et al1 (2018), where 910 patients followed up for 2 years, which showed that there was no significant difference between 3 groups in terms of anti-inflammation or prevention of coronary artery abnormalities. This paper concluded that the role of aspirin in the treatment of the acute phase of Kawasaki disease should be questioned, as a definite benefit has not been shown. Therefore, in concordance with the conclusion of the review, this rapid response poses that current data remains unchanged with regards to the role and effects of administration of higher doses of aspirin on coronary outcome in acute Kawasaki disease. In the absence of evidence to support higher doses in prevention of coronary artery abnormalities, low-dose aspirin (3–5 mg/kg) may be the safest, most rational approach until better evidence becomes available.
There are currently three prospective randomised control trials in process to continue this investigation2-4, it would be interesting to review this on their completion.
1. Huang, X. et al. Is aspirin necessary in the acute phase of Kawasaki disease? J. Paediatr. Child Health 54, 661–664 (2018).
2. NCT02951234. A Multi-center, Randomized to Compare the Efficacy of IVIG Alone and IVIG Plus High-dose Aspirin in Kawasaki Disease. Https://clinicaltrials.gov/show/nct02951234 doi:10.1002/CENTRAL/CN-01559692
3. NCT02359643. Multi-center Prospective Randomized Control Trail of High Dose Aspirin in Acute Stage of Kawasaki Disease. Https://clinicaltrials.gov/show/nct02359643 (2015). doi:10.1002/CENTRAL/CN-01582768
4. Kuo, H.-C., Guo, M. M.-H., Lo, M.-H., Hsieh, K.-S. & Huang, Y.-H. Effectiveness of intravenous immunoglobulin alone and intravenous immunoglobulin combined with high-dose aspirin in the acute stage of Kawasaki disease: study protocol for a randomized controlled trial. BMC Pediatr. 18, 200 (2018).
We thank Drs Bok et al. for their comments on our recent editorial about the use of palivizumab in children with Down syndrome (DS).[1] However, most of their arguments are not pertinent to DS. First, they describe the general incidence of respiratory syncytial virus (RSV) in children aged <5years. Second, they discuss the efficacy of palivizumab based on the IMpact trial [2] that did not include children with DS. We provided concrete evidence from [3] metanalyses conducted in 1.1 million children with DS, that the risk of RSV-related hospitalisation (RSVH) is 6.1–8.7- fold higher than children without DS.1 Drs Bok et al. also fail to appreciate that the overall relative risk of RSVH without palivizumab, is 5.5-fold (95% CI 3.97 to 7.7) higher based on robust, high quality evidence.[3] In our previous study we also reported that for every 1000 children with DS with RSV there will be 200 more (95% CI,131-297) hospitalisations compared with 1000 children without DS with RSV (RR, 5.53; 95% CI,3.97-7.73; high GRADE).[4] Moreover, Drs Bok et al. have extrapolated the number needed to treat (NNT) with prophylaxis to prevent one RSVH in children with DS using sub-optimal data. In a prospective case-control, cohort study conducted in the Netherlands and Canada, the estimated NNT in children with DS, adjusted for confounding variables, is 12 and not 20.[5] This number also aligns with the report from the CARESS registry [6] and compares favourably with the NNT of 16 for preter...
We thank Drs Bok et al. for their comments on our recent editorial about the use of palivizumab in children with Down syndrome (DS).[1] However, most of their arguments are not pertinent to DS. First, they describe the general incidence of respiratory syncytial virus (RSV) in children aged <5years. Second, they discuss the efficacy of palivizumab based on the IMpact trial [2] that did not include children with DS. We provided concrete evidence from [3] metanalyses conducted in 1.1 million children with DS, that the risk of RSV-related hospitalisation (RSVH) is 6.1–8.7- fold higher than children without DS.1 Drs Bok et al. also fail to appreciate that the overall relative risk of RSVH without palivizumab, is 5.5-fold (95% CI 3.97 to 7.7) higher based on robust, high quality evidence.[3] In our previous study we also reported that for every 1000 children with DS with RSV there will be 200 more (95% CI,131-297) hospitalisations compared with 1000 children without DS with RSV (RR, 5.53; 95% CI,3.97-7.73; high GRADE).[4] Moreover, Drs Bok et al. have extrapolated the number needed to treat (NNT) with prophylaxis to prevent one RSVH in children with DS using sub-optimal data. In a prospective case-control, cohort study conducted in the Netherlands and Canada, the estimated NNT in children with DS, adjusted for confounding variables, is 12 and not 20.[5] This number also aligns with the report from the CARESS registry [6] and compares favourably with the NNT of 16 for preterms <35 weeks gestation without bronchopulmonary dysplasia, 20 for children with bronchopulmonary dysplasia and 23 for those with congenital heart disease, based on randomised trials.
Last, regarding costs, Drs Bok et al. also fall short in their attempt to reconcile that palivizumab is not cost-effective in children with DS using data derived from preterm infants, which unfortunately has little relevance. In our editorial[1] and original report,[4] we emphasised that a well-conducted cost-utility analysis of RSV prophylaxis in children with DS that measures RSV-related disease burden on both the quality and quantity of life.is still lacking. What we do know from solid evidence is that the burden of illness associated with RSVH in children with DS and those without congenital heart disease compared to children without DS is significant,[1],[4] and is steadily increasing with concurrent healthcare expenditure.[7] Our editorial provides concrete information about the risks of RSVH in all children with DS while indicating that the real-world use of prophylaxis in this population is of greater benefit versus harm, and that non-intervention has significant clinical, healthcare costs and socioeconomic implications, the latter of which is often overlooked.[1],[8] After systematically weighing the pros and cons, we re-affirm that the time is right to consider RSV prophylaxis for all children with DS aged < 2 years, since the opposing data provided by Dr Bok et al. is at best hypothetical. However, we do agree that the adoption of a global policy for RSV prophylaxis in all children with DS must be balanced in each country against available funding, overall costs for RSVH and incurred short and long-term morbidity.
References
1 Paes B, Mitra S. Palivizumab for children with Down syndrome: is the time right for a universal recommendation? Arch Dis Child doi:10.1136/archdischild-2018-316408.
2 The IMpact-RSV Study Group. Palivizumab, a humanized respiratory syncytial virus monoclonal antibody, reduces hospitalization from respiratory syncytial virus infection in high-risk children. Pediatrics 1998; 102:531-7.
3 Guyatt GH, Oxman AD, Vist G, et al. GRADE guidelines: 4. Rating the quality of evidence—study limitations (risk of bias). J Clin Epidemiol 2011; 64:407-15.
4 Mitra S, El Azrak M, McCord H et al. Hospitalization for respiratory syncytial virus in children with Down syndrome less than 2 years of age: A systematic review and meta-analysis. J Pediatr. 2018; 203:92-100.e3.
5 Yi H, Lanctôt KL, Bont L, Bloemers BL, et al. Respiratory syncytial virus prophylaxis in Down syndrome: a prospective cohort study. Pediatrics 2014; 133:1031-7.
6 Paes B, Mitchell I, Yi H, et al. Hospitalization for respiratory syncytial virus illness in Down syndrome following prophylaxis with palivizumab. Pediatr Infect Dis J 2014; 33:e29-33.
7 Doucette A, Jiang X, Fryzek J, et al. Trends in respiratory syncytial virus and bronchiolitis hospitalization rates in high-risk infants in a United States nationally representative database, 1997-2012. PLoS One 2016; 11: e0152208.
8 Martínez-Valverde S, Salinas-Escudero G, García-Delgado C et al. Out-of-pocket expenditures and care time for children with Down Syndrome: A single-hospital study in Mexico City. PLoS One 2019;14:e0208076.
Many thanks for your response to the editorial ‘What are you looking at?’, which highlights some important principles for this extensively studied research area (despite being a relatively new field in healthcare) [1]
Despite the emergence of new methods to analyse gaze behaviour terminology has not been revised to reflect scientific advances. A recent article by Hessels et al. outlined significant inconsistencies in the definitions of fixations and saccades held by eye movement researchers and highlighted the conceptual confusion surrounding these terms.[2]
The term saccade is derived from the French for ‘jerk’. The phrase appears to have been coined by Emile Javal, a French ophthalmologist, in the 1800’s.[3] By 1916 it had been accepted into the English literature.[4]
Saccades are frequently defined in the literature as rapid, ballistic movements of the eyes that abruptly change the point of fixation.5 Definitions have included;
‘Rapid eye movements used to voluntarily move gaze from one target of interest to another.’[6]
‘Ballistic movements, 20-150ms long, reaching a velocity up to 800°/s. They direct the eye so that external visual objects are projected onto the fovea.’[7]
‘Rapid eye movements used in repositioning the fovea to a new location in the visual environment.’[8]
The term ballistic refers to the fact that the saccade-generating system cannot respond to subsequent changes in the position of a target during th...
Many thanks for your response to the editorial ‘What are you looking at?’, which highlights some important principles for this extensively studied research area (despite being a relatively new field in healthcare) [1]
Despite the emergence of new methods to analyse gaze behaviour terminology has not been revised to reflect scientific advances. A recent article by Hessels et al. outlined significant inconsistencies in the definitions of fixations and saccades held by eye movement researchers and highlighted the conceptual confusion surrounding these terms.[2]
The term saccade is derived from the French for ‘jerk’. The phrase appears to have been coined by Emile Javal, a French ophthalmologist, in the 1800’s.[3] By 1916 it had been accepted into the English literature.[4]
Saccades are frequently defined in the literature as rapid, ballistic movements of the eyes that abruptly change the point of fixation.5 Definitions have included;
‘Rapid eye movements used to voluntarily move gaze from one target of interest to another.’[6]
‘Ballistic movements, 20-150ms long, reaching a velocity up to 800°/s. They direct the eye so that external visual objects are projected onto the fovea.’[7]
‘Rapid eye movements used in repositioning the fovea to a new location in the visual environment.’[8]
The term ballistic refers to the fact that the saccade-generating system cannot respond to subsequent changes in the position of a target during the course of an eye movement. If the target was to move a second saccade would be required to correct the error. Acceptance of such definitions suggests that the primary function of saccades is to bring objects of interest onto or near the fovea. The fovea operates at high resolution and, although it only provides 1-2 degrees of vision, it plays a central role in resolving objects. Whilst saccades assist vision by moving the eyes rapidly to various objects of interest so that parts of a scene can be seen in greater resolution, there is probably little or no meaningful information absorbed during the saccadic movements.
However, other papers have been more liberal in their definitions defining a saccade as the inter-fixation interval.[9,10] These definitions imply that a saccade is any movement outside of periods of fixation. This definition will therefore also capture smooth pursuit movements (slower tracking movements), vestibulo-ocular movements (stabilise eyes relative to external world) and visual scanning movements. Consequentially during saccades defined in this manner visual information may be absorbed both consciously and/or subconsciously including, for example, the presence or absence of pathology, as outlined in your letter.
As the field of eye tracking research in healthcare expands it is imperative that authors explicitly define their key measurements, including fixations, dwell time and saccades, to allow accurate interpretation and comparison of results and to minimise ambiguity. Without this it will be difficult to examine the links between visual scanning patterns and decision making. For example it may be hypothesised that subconscious visual scanning behaviours may be a clue to understanding the concept of gut feeling, whereby a particular clinician sees things perhaps others do not.
We certainly agree greater understanding of saccade pathways should undoubtedly be an area for future research in eye tracking studies in healthcare.
References:
1. Roland D. What are you looking at? Arch Dis Child 2018; 103: 1098-1099.
2. Hessels RS, Niehorster DC, Nyström M, Andersson R, Hooge IT. Is the eye-movement field confused about fixations and saccades? A survey among 124 researchers. Royal Society open science. 2018 Aug 29;5(8):180502.
3. Javal E. Essai sur la physiologie de la lecture. Annales d'Ocilistique. 1878;80:61-73.
4. Wade NJ. Scanning the seen: Vision and the origins of eye-movement research. In Eye Movements 2007 (pp. 31-63).
5. Purves D, Augustine GJ, Fitzpatrick D, Katz LC, LaMantia AS, McNamara JO, Williams SM. Neuroscience 2nd Edition. Sunderland (MA) Sinauer Associates.
6. Ramat S, Leigh RJ, Zee DS, Optican LM. What clinical disorders tell us about the neural control of saccadic eye movements. Brain. 2006 Nov 21;130(1):10-35.
7. Falkmer T, Dahlman J, Dukic T, Bjällmark A, Larsson M. Fixation identification in centroid versus start-point modes using eye-tracking data. Perceptual and motor skills. 2008 Jun;106(3):710-24.
8. Duchowski AT. Eye tracking methodology. Theory and practice. 2007;328.
9. Holmqvist K, Nyström M, Andersson R, Dewhurst R, Jarodzka H, Van de Weijer J. Eye tracking: A comprehensive guide to methods and measures. OUP Oxford; 2011 Sep 22.
10. Larsson L, Nyström M, Andersson R, Stridh M. Detection of fixations and smooth pursuit movements in high-speed eye-tracking data. Biomedical Signal Processing and Control. 2015 Apr 1;18:145-52.
We thank Nitzan et al for their comments in relation to our article on use of pulsatility index (PI) in screening for critical congenital heart disease (Searle 2018). In particular, we are grateful that they draw further attention to the potential for current screening to miss critical lesions, such as coarctation of the aorta. Given the progressive nature of these pathologies, it is an extremely difficult challenge to design an acceptable screening tool, which highlights all affected babies in appropriate time. Despite strong biological plausibility, current evidence is unclear whether pulsatility index can translate into such a tool.
We fully agree that the local quality of both antenatal and postnatal screening significantly affects the measured benefit of pulsatility index. Several articles draw the distinction here between ‘tertiary’ and ‘non-tertiary’ units, though it may be more accurate to distinguish ‘better resourced’ from ‘less resourced’ settings, particularly in relation to antenatal scanning. As described in our original article, the apparent potential of PI screening in ‘less resourced’ settings seems strong, especially since many pulse oximetry sensors already measure it. Both Schena et al (2017) and Granelli & Ostman-Smith (2007) highlight a small but important population of babies not detected by standard screening, but with abnormal pre-morbid pulsatility indices. It seems incongruous, however, to extrapolate a single extra case detected by th...
We thank Nitzan et al for their comments in relation to our article on use of pulsatility index (PI) in screening for critical congenital heart disease (Searle 2018). In particular, we are grateful that they draw further attention to the potential for current screening to miss critical lesions, such as coarctation of the aorta. Given the progressive nature of these pathologies, it is an extremely difficult challenge to design an acceptable screening tool, which highlights all affected babies in appropriate time. Despite strong biological plausibility, current evidence is unclear whether pulsatility index can translate into such a tool.
We fully agree that the local quality of both antenatal and postnatal screening significantly affects the measured benefit of pulsatility index. Several articles draw the distinction here between ‘tertiary’ and ‘non-tertiary’ units, though it may be more accurate to distinguish ‘better resourced’ from ‘less resourced’ settings, particularly in relation to antenatal scanning. As described in our original article, the apparent potential of PI screening in ‘less resourced’ settings seems strong, especially since many pulse oximetry sensors already measure it. Both Schena et al (2017) and Granelli & Ostman-Smith (2007) highlight a small but important population of babies not detected by standard screening, but with abnormal pre-morbid pulsatility indices. It seems incongruous, however, to extrapolate a single extra case detected by the Schena et al (2017) study into a real 50% improvement in detection rates, over pulse oximetry screening alone. With such small numbers, the difference between an important finding and statistical or technical anomaly is impossible to determine. We hope this clarifies our original statement that ‘current evidence does not support inclusion of PI into newborn screening’.
Moving forward, the inclusion of pulsatility index within current screening practice would require further large population studies, particularly looking at babies within ‘less resourced’ settings. To make such a study acceptable, the methodology must either i) reduce the high false-positive rate (typically 5%) associated with previous approaches or ii) have robust and pragmatic mechanisms to safely minimise the impact of a false-positive screen on a newborn and their family. Use of different technologies may address the former requirement. Pre-to-post ductal pulse delay, for example, is an innovative approach, though it is untested within a screening context (Palmeri 2017). Within this study, all ‘case’ group babies already demonstrated significant clinical signs at time of testing. Similarly, Nitzan et al’s suggestion to repeat PI measurement after a few days has merit. Establishing the optimal timing of measurements however would be a challenge, to maximise detection without missing early cases. Granelli & Ostman-Smith (2007) could not answer this point, despite study of 10,000 babies up to day 5 of life.
It seems unacceptable to remain in the status quo, where a significant portion of babies are only detected following life-threatening collapse. PI could be an important addition to the screening armoury in ‘low resourced’ settings, but true population-specific evidence would be needed. We very much welcome an open discussion of how to overcome the challenges this would pose.
REFERENCES
Granelli A, Ostman-Smith I. Noninvasive peripheral perfusion index as a possible tool for screening for critical left heart obstruction. Acta Paediatr. 2007;96:1455–9
Palmeri L, Gradwohl G, Nitzan M, et al. Photoplethysmographic waveform characteristics of newborns with coarctation of the aorta. J Perinatol. 2017;37:77–80
Schena F, Picciolli I, Agosti M, et al. Perfusion index and pulse oximetry screening for congenital heart defects. J Pediatr. 2017;183:74–9
The review by Searle et al “Does pulsatility index add value to newborn pulse oximetry screening for critical congenital heart disease?" (Searle 2018), provides a comprehensive overview of the current evidence regarding the addition of perfusion index to the CCHD screening algorithm.
The authors’ main concern is that adding pulsatility index (perfusion index, PI) will not significantly improve the current detection rate which is already quite high. As a proof, they cite the work of the large trial by Schena et al, (Schena 2017) that found one additional case of CCHD in 42,169 babies examined. The authors conclude that incorporating PI into current screening algorithms provides little additional benefit in detecting CCHD and confers a high false positive rate.
We would like to voice several comments regarding this article:
First, in the study of Schena et al, CCHD was suspected before screening in 36/38 cases in tertiary centers. This is the main reason that PI (and pulse oximetry screening) did not have any additional value in tertiary centers. In this study, only 23.6% of the neonates were born in non-tertiary center. We suggest that an alternative way to describe the results is that in non-tertiary centers, pulse oximetry detected 2 cases and PI detected an additional 1 case per approximately 10,000 screened neonates. Therefore, adding PI to the screening algorithm improved the detection rate by 50%. Moreover, the 2 cases detected by pulse oximetry...
The review by Searle et al “Does pulsatility index add value to newborn pulse oximetry screening for critical congenital heart disease?" (Searle 2018), provides a comprehensive overview of the current evidence regarding the addition of perfusion index to the CCHD screening algorithm.
The authors’ main concern is that adding pulsatility index (perfusion index, PI) will not significantly improve the current detection rate which is already quite high. As a proof, they cite the work of the large trial by Schena et al, (Schena 2017) that found one additional case of CCHD in 42,169 babies examined. The authors conclude that incorporating PI into current screening algorithms provides little additional benefit in detecting CCHD and confers a high false positive rate.
We would like to voice several comments regarding this article:
First, in the study of Schena et al, CCHD was suspected before screening in 36/38 cases in tertiary centers. This is the main reason that PI (and pulse oximetry screening) did not have any additional value in tertiary centers. In this study, only 23.6% of the neonates were born in non-tertiary center. We suggest that an alternative way to describe the results is that in non-tertiary centers, pulse oximetry detected 2 cases and PI detected an additional 1 case per approximately 10,000 screened neonates. Therefore, adding PI to the screening algorithm improved the detection rate by 50%. Moreover, the 2 cases detected by pulse oximetry did not have ductal dependent systemic circulation. Therefore, the most important detection in this study was by PI. We agree with the authors that pulse oximetry CCHD screening, with or without PI, has a low detection rate in tertiary units. However, we believe that this study demonstrates the potential utility of PI as a supplementary screening method in non-tertiary units. This information may be of value in regions with limited access to fetal diagnosis which is expensive and requires advanced technical skills while PI is inexpensive and may be performed by nurses and midwives.
Second, we would like to draw attention to the three missed cases of critical left-sided obstruction described in this study. Two of the neonates presented with signs of shock and cardiac failure. We believe that the current screening algorithms may be improved by measuring the pulse wave delay between extremities (Palmeri 2017) as was mentioned in the review. Detection rates may also increase by improving the method of derivation of PI and by comparing pre and post-ductal PI values (Palmeri 2017, Nitzan 2018). Another option that may be relevant in some regions, is a repeated screening test performed in the community clinic or during a home visit after hospital discharge in the hope of detecting critical left-sided obstruction during the process of duct closure before the onset of cardiac failure.
We thank the authors for raising awareness of this important question, and we hope that future studies will address this issue.
Searle J, Thakkar DD, Banerjee J.Does pulsatility index add value to newborn pulse oximetry screening for critical congenital heart disease? Arch Dis Child. 2018 Nov 9. pii: archdischild-2018-315891. doi: 10.1136/archdischild-2018-315891. [Epub ahead of print]
Schena F, Picciolli I, Agosti M, et al. Perfusion index and pulse oximetry screening for
congenital heart defects. J Pediatr 2017;183:74–9.
Palmeri L, Gradwohl G, Nitzan M, et al. Photoplethysmographic waveform
characteristics of newborns with coarctation of the aorta. J Perinatol 2017;37:77–80.
Nitzan I, Hammerman C, Fink D, Nitzan M, Koppel R, Bromiker R. The effect of patent ductus arteriosus on pre-ductal and post-ductal perfusion index in preterm neonates. Physiol Meas. 2018 Jul 20;39(7):075006. doi: 10.1088/1361-6579/aacf25.
Seo et al. conducted a prospective study to identify factors for cardiovascular disease risk factor clustering (CVD-RFC) in adolescents (1). A total of 1309 children aged 6-15 years were enrolled, and higher household income was a significant predictor of lower CVD-RFC incidence with dose-response relationship. In contrast, the presence of parental CVD history, overweight or obesity, and shorter sleep duration were significant predictors of higher CVD-RFC incidence. I have some comments with special reference to socioeconomic status (SES) and metabolic components.
First, Iguacel et al. investigated the association between socioeconomic disadvantages and metabolic syndrome (MetS) in children (2). By adjusting diet, physical activity, sedentary behaviours and well-being, standardized multiple regression coefficients (99% confidence intervals [CI]) of children from low-income families, non-traditional families, with parents of unemployment, and accumulation of >3 socioeconomic disadvantages for a higher MetS score were 0.20 (0.03-0.37), 0.14 (0.02-0.26), 0.31 (0.05-0.57), 0.21 (0.04-0.37), respectively. These data present that low SES was closely associated with MetS in children, which was in concordance with data by Seo et al (1).
Second, Patel et al. examined the association between parental socioeconomic position (SEP) and early-life offspring body mass index (BMI) in children (3). Adjusted difference of BMI z-score (95% CI) was 0.08 (0-0.16) among girls...
Seo et al. conducted a prospective study to identify factors for cardiovascular disease risk factor clustering (CVD-RFC) in adolescents (1). A total of 1309 children aged 6-15 years were enrolled, and higher household income was a significant predictor of lower CVD-RFC incidence with dose-response relationship. In contrast, the presence of parental CVD history, overweight or obesity, and shorter sleep duration were significant predictors of higher CVD-RFC incidence. I have some comments with special reference to socioeconomic status (SES) and metabolic components.
First, Iguacel et al. investigated the association between socioeconomic disadvantages and metabolic syndrome (MetS) in children (2). By adjusting diet, physical activity, sedentary behaviours and well-being, standardized multiple regression coefficients (99% confidence intervals [CI]) of children from low-income families, non-traditional families, with parents of unemployment, and accumulation of >3 socioeconomic disadvantages for a higher MetS score were 0.20 (0.03-0.37), 0.14 (0.02-0.26), 0.31 (0.05-0.57), 0.21 (0.04-0.37), respectively. These data present that low SES was closely associated with MetS in children, which was in concordance with data by Seo et al (1).
Second, Patel et al. examined the association between parental socioeconomic position (SEP) and early-life offspring body mass index (BMI) in children (3). Adjusted difference of BMI z-score (95% CI) was 0.08 (0-0.16) among girls and 0.16 (0.07-0.24) among boys, and they concluded that higher SEP was associated with greater BMI trajectories in both sexes. In contrast, Oddo and Jones-Smith investigated the association between the change of family income and the change of BMI z-score in children (4). The poverty to family income ratio (PIR) and the increase in PIR were significantly associated with decrease in BMI z-score only among girls. Seo et al. did not recognize significant sex difference, but they presented 10% decrease of CVD-RFC in girls. Sex difference should be specified by further study.
Finally, Lee et al. investigate the relationship between SES and obesity in children (5). They used education and income as an indicator of SES, and SES was not a significant indicator for childhood obesity. In contrast, childhood obesity was positively associated with maternal overweight, maternal obesity and paternal obesity. SES had a smaller impact than parental obesity on childhood obesity. Relating to this report, Andrea et al. conducted a systematic review concerning the effect of early life growth (0-24 months of age) on later obesity (>24 months) by considering race/ethnicity and SES (6). They recognized that the positive association was predominant in populations of racial/ethnic minority. A comprehensive analysis is needed to identify the association between SES and CVD-RFC.
References
1 Seo YG, Choi MK, Kang JH, et al. Cardiovascular disease risk factor clustering in children and adolescents: a prospective cohort study. Arch Dis Child 2018;103:968-73
2 Iguacel I, Michels N, Ahrens W, et al. Prospective associations between socioeconomically disadvantaged groups and metabolic syndrome risk in European children. Results from the IDEFICS study. Int J Cardiol 2018:272 :333-40.
3 Patel R, Tilling K, Lawlor DA, et al. Socioeconomic differences in childhood BMI trajectories in Belarus. Int J Obes (Lond) 2018:42:1651-60.
4 Oddo VM, Jones-Smith JC. Gains in income during early childhood are associated with decreases in BMI z scores among children in the United States. Am J Clin Nutr 2015;101:1225-31.
5 Lee HJ, Kim SH, Choi SH, et al. The Association between socioeconomic status and obesity in Korean children: An analysis of the Fifth Korea National Health and Nutrition Examination Survey (2010-2012). Pediatr Gastroenterol Hepatol Nutr 2017;20:186-93.
6 Andrea SB, Hooker ER, Messer LC, et al. Does the association between early life growth and later obesity differ by race/ethnicity or socioeconomic status? A systematic review. Ann Epidemiol 2017;27:583-92.e5.
It is with great interest that we read ‘Why do babies cry?” in which Dr. Robert Scott-Jupp have provided a concise evaluation of the research pertaining to non-pathologic crying in infants.
Crying is a normal variant in the day 2 newborn examination however it can pose a significant source of stress and anxiety for parents. To add to the body of evidence detailed in this article we posed the question; What proportion of babies cry during the day 2 newborn examination?
A convenience sample of data was collected on well babies during the standard day 2 physical examination on the postnatal ward in a tertiary maternity hospital. All babies on the postnatal ward were eligible for inclusion. Gestation, birth weight, gender, mode of delivery and duration of examination were recorded. The presence or absence of crying during examination was documented. The data was analysed using SPSS .
One hundred and fifty three babies (n=153) were included in the study. There were 82 male infants (53%) and 71 female infants (47%). Mean birth weight was 3589g (range 2590g -5160g) with a mean gestation of 39+4 (Range 36+3 - 42+1). Mean duration of examination was 7 minutes. Eighty-one babies (52.9%) delivered by spontaneous vaginal delivery, 22 (14.4%) by ventouse, 26 (16.9%) by elective caesarean section, 20 (13.1%) by emergency caesarean section and 4(2.6%) by forceps. Overall, 118 (77.1%) babies were observed to cry during the physical examination (78%...
It is with great interest that we read ‘Why do babies cry?” in which Dr. Robert Scott-Jupp have provided a concise evaluation of the research pertaining to non-pathologic crying in infants.
Crying is a normal variant in the day 2 newborn examination however it can pose a significant source of stress and anxiety for parents. To add to the body of evidence detailed in this article we posed the question; What proportion of babies cry during the day 2 newborn examination?
A convenience sample of data was collected on well babies during the standard day 2 physical examination on the postnatal ward in a tertiary maternity hospital. All babies on the postnatal ward were eligible for inclusion. Gestation, birth weight, gender, mode of delivery and duration of examination were recorded. The presence or absence of crying during examination was documented. The data was analysed using SPSS .
One hundred and fifty three babies (n=153) were included in the study. There were 82 male infants (53%) and 71 female infants (47%). Mean birth weight was 3589g (range 2590g -5160g) with a mean gestation of 39+4 (Range 36+3 - 42+1). Mean duration of examination was 7 minutes. Eighty-one babies (52.9%) delivered by spontaneous vaginal delivery, 22 (14.4%) by ventouse, 26 (16.9%) by elective caesarean section, 20 (13.1%) by emergency caesarean section and 4(2.6%) by forceps. Overall, 118 (77.1%) babies were observed to cry during the physical examination (78% male vs 76% female). There was no difference in incidence of crying when compared for gestation. Eighty eight percent of babies born by instrumental delivery cried during examination while only 74% of those born by spontaneous vaginal delivery and 76% of those born by emergency section cried. Babies with a birth weight of 4001g – 4500g were more likely to cry than any other birth weight category (90.4%).
To conclude, crying is a normal variant in the newborn examination. Communicating these statistics to parents could play a role in reducing stress and anxiety. This is the first study to document the frequency of crying on the day 2 examination. It was also observed that babies of a higher birth weight, as well as those delivered instrumentally, were more likely to cry than others.
As a final year medical student, I read with great interest this article highlighting the pedagogical value of gaze study. Whilst the article raises many poignant features of this new medium of data collection, I believe the definition of saccade in your article may be slightly incomplete.
The article states that “Saccades...are movements of the eyes between fixations in which information is not meaningfully acquired or absorbed.” However, I would suggest that whilst the primary purpose of saccades may be to move between fixation points, there is subconscious information acquisition completed by these movements-- the subconscious identification of a lack of pathology.
If one does not take certain regions of an image as fixation points, it suggests that they are not looking for pathology in those regions. This is reinforced by one study analysing gaze study in mammogram analysis which reported that “long saccades often missed the target but were followed by corrective saccades”. (1-Kundel H, Nodine C, Conant E et al. Holistic component of image perception in mammogram interpretation: gaze-tracking study. Radiology 2007;242(2):396-402.) This highlights that within a saccade is also inert analysis of a lack of pathology rather than just transformational eye movement.
Another study analysing a gaze study of virtual histopathology slides between trained pathologists, residents and medical students reported that “fully trained pathologists h...
As a final year medical student, I read with great interest this article highlighting the pedagogical value of gaze study. Whilst the article raises many poignant features of this new medium of data collection, I believe the definition of saccade in your article may be slightly incomplete.
The article states that “Saccades...are movements of the eyes between fixations in which information is not meaningfully acquired or absorbed.” However, I would suggest that whilst the primary purpose of saccades may be to move between fixation points, there is subconscious information acquisition completed by these movements-- the subconscious identification of a lack of pathology.
If one does not take certain regions of an image as fixation points, it suggests that they are not looking for pathology in those regions. This is reinforced by one study analysing gaze study in mammogram analysis which reported that “long saccades often missed the target but were followed by corrective saccades”. (1-Kundel H, Nodine C, Conant E et al. Holistic component of image perception in mammogram interpretation: gaze-tracking study. Radiology 2007;242(2):396-402.) This highlights that within a saccade is also inert analysis of a lack of pathology rather than just transformational eye movement.
Another study analysing a gaze study of virtual histopathology slides between trained pathologists, residents and medical students reported that “fully trained pathologists had prolonged saccadic movement and lower saccadic velocity [compared to residents and medical students]”. (2-Krupinski E, Tillack A, Richter L et al. Eye-movement study and human performance using telepathology virtual slides. Implications for medical education and differences with experience. Hum Pathol 2006;37(12):1543-56.) This suggests that experts do not need to have greater fixation points as they were aware of a lack of pathology through subconscious processing which led to a lower saccade velocity.
Through greater understanding about saccade pathways, we may be able to both add to our knowledge of how participants are analysing the data they are being given as well as position ourselves to better analyse where participants are also missing pathology.
We thank Professor Marchetti for his comments on our article in ADC (1). He raises two important questions we wish to comment on.
Regarding which dose of aspirin to use, we are also interested in the suggestion that anti-aggregant doses of aspirin might be a preferred option for the acute inflammatory phase of Kawasaki disease (KD). It is indeed possible that future guidance may recommend low dose aspirin (3-5 mg/kg/day) at all stages of KD, as suggested by the retrospective data referred to by Professor Marchetti (2). Whilst we acknowledge the potential merits of such an approach, particularly in relation to avoidance of toxicity, there has never been a prospective controlled clinical trial to support this and therefore no high-level evidence on which to base firm guidance. Two other practical considerations are worthy of highlighting in relation to aspirin. Firstly, nonsteroidal anti-inflammatory drugs such as ibuprofen, which antagonize platelet inhibition induced by aspirin (3), should be avoided in patients with KD receiving anti-aggregant doses of aspirin. Secondly, although the risk of low dose aspirin (3-5 mg/kg) in being associated with Reye syndrome is unknown, usual advice is to discontinue in the event of inter-current infection.
Regarding the use of corticosteroids for primary treatment of KD, we have been strong advocates of this for several years, as reflected in previously published guidance (4, 5). This is now brought into...
We thank Professor Marchetti for his comments on our article in ADC (1). He raises two important questions we wish to comment on.
Regarding which dose of aspirin to use, we are also interested in the suggestion that anti-aggregant doses of aspirin might be a preferred option for the acute inflammatory phase of Kawasaki disease (KD). It is indeed possible that future guidance may recommend low dose aspirin (3-5 mg/kg/day) at all stages of KD, as suggested by the retrospective data referred to by Professor Marchetti (2). Whilst we acknowledge the potential merits of such an approach, particularly in relation to avoidance of toxicity, there has never been a prospective controlled clinical trial to support this and therefore no high-level evidence on which to base firm guidance. Two other practical considerations are worthy of highlighting in relation to aspirin. Firstly, nonsteroidal anti-inflammatory drugs such as ibuprofen, which antagonize platelet inhibition induced by aspirin (3), should be avoided in patients with KD receiving anti-aggregant doses of aspirin. Secondly, although the risk of low dose aspirin (3-5 mg/kg) in being associated with Reye syndrome is unknown, usual advice is to discontinue in the event of inter-current infection.
Regarding the use of corticosteroids for primary treatment of KD, we have been strong advocates of this for several years, as reflected in previously published guidance (4, 5). This is now brought into sharp focus in the light of emerging data from several countries regarding poor coronary artery outcomes despite Intravenous immunoglobulin (IVIG) (1, 6-9). Indeed, the use of corticosteroids as primary adjunctive treatment of patients with severe KD has an increasingly compelling evidence-base. Despite that and UK guidance that was published halfway during the BPSU survey (5), our study demonstrates that UK paediatricians are not yet widely using corticosteroids for the treatment of KD (1). The soon-to-be published European SHARE (single hub access for rheumatology in Europe) guidance hopefully will improve that situation for high risk cases, but there clearly remains significant equipoise over the use of corticosteroids as adjunctive therapy for unselected cases of KD. Thus, at the time of writing we are currently setting up a major international clinical trial of corticosteroids as adjunctive treatment for unselected KD cases in the UK and Europe, KDCAAP (the Kawasaki Disease Coronary Artery Aneurysm Prevention trial). It is possible that the added potent anti-inflammatory effect of adjunctive corticosteroids for the primary treatment of KD will obviate the need for any further discussion about anti-inflammatory doses of aspirin. We hope that the UK and European paediatric community will recruit patients to this important clinical trial to resolve this issue once and for all.
Professor Robert Tulloh, Bristol Royal Hospital for Children, Bristol, UK
Professor Paul Brogan, Great Ormond Street Hospital, London, UK
1. Tulloh RMR, Mayon-White R, Harnden A, Ramanan AV, Tizard EJ, Shingadia D, Michie CA, Lynn RM, Levin M, Franklin OD, Craggs P, Davidson S, Stirzaker R, Danson M, Brogan PA. Kawasaki disease: a prospective population survey in the UK and Ireland from 2013 to 2015. Archives of Disease in Childhood. 2018.
2. Ho LGY, Curtis N. What dose of aspirin should be used in the initial treatment of Kawasaki disease? Archives of Disease in Childhood. 2017;102(12):1180-2.
3. Catella-Lawson F, Reilly MP, Kapoor SC, Cucchiara AJ, DeMarco S, Tournier B, Vyas SN, FitzGerald GA. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med. 2001;345(25):1809-17.
4. Brogan PA, Bose A, Burgner D, Shingadia D, Tulloh R, Michie C, Klein N, Booy R, Levin M, Dillon MJ. Kawasaki disease: an evidence based approach to diagnosis, treatment, and proposals for future research. Arch Dis Child. 2002;86(4):286-90.
5. Eleftheriou D, Levin M, Shingadia D, Tulloh R, Klein NJ, Brogan PA. Management of Kawasaki disease. Arch Dis Child. 2014;99(1):74-83.
6. Mossberg M, Segelmark M, Kahn R, Englund M, Mohammad AJ. Epidemiology of primary systemic vasculitis in children: a population-based study from southern Sweden. Scand J Rheumatol. 2018;47(4):295-302.
7. Lyskina G, Bockeria O, Shirinsky O, Torbyak A, Leontieva A, Gagarina N, Satyukova A, Kostina J, Vinogradova O. Cardiovascular outcomes following Kawasaki disease in Moscow, Russia: A single center experience. Global cardiology science & practice. 2017;2017(3):e201723.
8. Jakob A, Whelan J, Kordecki M, Berner R, Stiller B, Arnold R, von KR, Neumann E, Roubinis N, Robert M, Grohmann J, Hohn R, Hufnagel M. Kawasaki Disease in Germany: A Prospective, Population-based Study Adjusted for Underreporting. Pediatr Infect Dis J. 2016;35(2):129-34.
9. Friedman KG, Gauvreau K, Hamaoka-Okamoto A, Tang A, Berry E, Tremoulet AH, Mahavadi VS, Baker A, deFerranti SD, Fulton DR, Burns JC, Newburger JW. Coronary Artery Aneurysms in Kawasaki Disease: Risk Factors for Progressive Disease and Adverse Cardiac Events in the US Population. Journal of the American Heart Association. 2016;5(9).
We thank you for the opportunity to discuss our data with the two correspondents who raised some concerns regarding the selected population of our analysis on neonatal outcomes following new reimbursement criteria on palivizumab use. They also reported data collected during the same time period and apparently different from our main results.
In response to the first correspondent, our analysis is based on children < 2 years of age because the candidate for palivizumab treatments are included within this subpopulation. In fact, the therapeutic indication (1) of palivizumab includes not only the preterm infants up to 1 year of age but also children up to 2 years of age and treated for bronchopulmonary dysplasia or born with a serious heart disease. Furthermore, our selected population is consistent with previous analysis (2) that measured the association between updated guidelines-based palivizumab administration and hospitalization for Respiratory Syncytial Virus (RSV). Table 1 of our study reports children up to 6 months of age, both at risk of RSV and including hospitalization data. We agree that this is probably the subpopulation with the major impact of the palivizumab treatment and regulatory decision. However, also in this case no differences in hospitalization rate have been detected before-after the AIFA’ limitation for palivizumab: 1031/47.608 (21.7 ‰) and 436/22715 (19.2 ‰) hospitalizations, respectiv...
We thank you for the opportunity to discuss our data with the two correspondents who raised some concerns regarding the selected population of our analysis on neonatal outcomes following new reimbursement criteria on palivizumab use. They also reported data collected during the same time period and apparently different from our main results.
In response to the first correspondent, our analysis is based on children < 2 years of age because the candidate for palivizumab treatments are included within this subpopulation. In fact, the therapeutic indication (1) of palivizumab includes not only the preterm infants up to 1 year of age but also children up to 2 years of age and treated for bronchopulmonary dysplasia or born with a serious heart disease. Furthermore, our selected population is consistent with previous analysis (2) that measured the association between updated guidelines-based palivizumab administration and hospitalization for Respiratory Syncytial Virus (RSV). Table 1 of our study reports children up to 6 months of age, both at risk of RSV and including hospitalization data. We agree that this is probably the subpopulation with the major impact of the palivizumab treatment and regulatory decision. However, also in this case no differences in hospitalization rate have been detected before-after the AIFA’ limitation for palivizumab: 1031/47.608 (21.7 ‰) and 436/22715 (19.2 ‰) hospitalizations, respectively. As in our main analysis, we were not able to see an increase of hospitalization related to the new reimbursement decision but a significant reduction (p=0.033) that we assume could be related to a more accurate coding by hospital or with an increase for palivizumab compliance in babies with higher risk of RSV infections.
In the second letter the authors presented data from three different hospitals supporting hypothetical opposite trend in hospitalization compared with our results. However, data from two of the three hospitals are related to general cases of bronchiolitis not specifically associated with RSV. None of the three separate groups of patients have statistically significant differences between the considered periods. Furthermore, these data do not take into account the potential mobility of all patients from one hospital to another. The subjects included in our analysis come for 70% of cases by the same three hospitals located in Rome quoted by the correspondents; all others patients are from regional hospitals where patients may receive assistance under the regional health coverage. From our point of view this give a better and comprehensive prospective compared to single hospital analysis.
We recognise in the limitations of the study that our ecological analysis was not able to measure the impact on specific subpopulations and administrative data can lose some clinically relevant information.
However, we cannot understand how the data presented in these correspondences can be considered more real than those collected in our study and to disprove our conclusions.
Antonio Addis, Valeria Belleudi
Department of Epidemiology, Lazio Regional Health Service, Roma, Italy
1. European Medicine Agency - Synagis : EPAR - Product Information https://www.ema.europa.eu/documents/product-information/synagis-epar-product-information_en.pdf
2. Grindeland CJ, Mauriello CT, Leedahl DD, et al. Association Between Updated Guideline-Based Palivizumab Administration and Hospitalizations for Respiratory Syncytial Virus Infections. Pediatr Infect Dis J 2016;35:728–32.doi:10.1097/INF.0000000000001150Google Scholar
Sir,
I would like to add to the article ‘What dose of aspirin should be used in the initial treatment of Kawasaki disease?’ by Luke Guo Yang Ho and Nigel Curtis (Archives, 2017, 102, 1180-1182). Fifteen months have passed since this article concluded that low-dose aspirin is not inferior to higher doses in reducing the risk of coronary artery abnormalities in acute Kawasaki disease. Since then, it is worth considering what and if anything has changed in the field. A recent study not included in the review is a retrospective cohort study by Huang et al1 (2018), where 910 patients followed up for 2 years, which showed that there was no significant difference between 3 groups in terms of anti-inflammation or prevention of coronary artery abnormalities. This paper concluded that the role of aspirin in the treatment of the acute phase of Kawasaki disease should be questioned, as a definite benefit has not been shown. Therefore, in concordance with the conclusion of the review, this rapid response poses that current data remains unchanged with regards to the role and effects of administration of higher doses of aspirin on coronary outcome in acute Kawasaki disease. In the absence of evidence to support higher doses in prevention of coronary artery abnormalities, low-dose aspirin (3–5 mg/kg) may be the safest, most rational approach until better evidence becomes available.
There are currently three prospective randomised control trials in process to continue this inv...
Show MoreWe thank Drs Bok et al. for their comments on our recent editorial about the use of palivizumab in children with Down syndrome (DS).[1] However, most of their arguments are not pertinent to DS. First, they describe the general incidence of respiratory syncytial virus (RSV) in children aged <5years. Second, they discuss the efficacy of palivizumab based on the IMpact trial [2] that did not include children with DS. We provided concrete evidence from [3] metanalyses conducted in 1.1 million children with DS, that the risk of RSV-related hospitalisation (RSVH) is 6.1–8.7- fold higher than children without DS.1 Drs Bok et al. also fail to appreciate that the overall relative risk of RSVH without palivizumab, is 5.5-fold (95% CI 3.97 to 7.7) higher based on robust, high quality evidence.[3] In our previous study we also reported that for every 1000 children with DS with RSV there will be 200 more (95% CI,131-297) hospitalisations compared with 1000 children without DS with RSV (RR, 5.53; 95% CI,3.97-7.73; high GRADE).[4] Moreover, Drs Bok et al. have extrapolated the number needed to treat (NNT) with prophylaxis to prevent one RSVH in children with DS using sub-optimal data. In a prospective case-control, cohort study conducted in the Netherlands and Canada, the estimated NNT in children with DS, adjusted for confounding variables, is 12 and not 20.[5] This number also aligns with the report from the CARESS registry [6] and compares favourably with the NNT of 16 for preter...
Show MoreMany thanks for your response to the editorial ‘What are you looking at?’, which highlights some important principles for this extensively studied research area (despite being a relatively new field in healthcare) [1]
Despite the emergence of new methods to analyse gaze behaviour terminology has not been revised to reflect scientific advances. A recent article by Hessels et al. outlined significant inconsistencies in the definitions of fixations and saccades held by eye movement researchers and highlighted the conceptual confusion surrounding these terms.[2]
The term saccade is derived from the French for ‘jerk’. The phrase appears to have been coined by Emile Javal, a French ophthalmologist, in the 1800’s.[3] By 1916 it had been accepted into the English literature.[4]
Saccades are frequently defined in the literature as rapid, ballistic movements of the eyes that abruptly change the point of fixation.5 Definitions have included;
‘Rapid eye movements used to voluntarily move gaze from one target of interest to another.’[6]
‘Ballistic movements, 20-150ms long, reaching a velocity up to 800°/s. They direct the eye so that external visual objects are projected onto the fovea.’[7]
‘Rapid eye movements used in repositioning the fovea to a new location in the visual environment.’[8]
The term ballistic refers to the fact that the saccade-generating system cannot respond to subsequent changes in the position of a target during th...
Show MoreWe thank Nitzan et al for their comments in relation to our article on use of pulsatility index (PI) in screening for critical congenital heart disease (Searle 2018). In particular, we are grateful that they draw further attention to the potential for current screening to miss critical lesions, such as coarctation of the aorta. Given the progressive nature of these pathologies, it is an extremely difficult challenge to design an acceptable screening tool, which highlights all affected babies in appropriate time. Despite strong biological plausibility, current evidence is unclear whether pulsatility index can translate into such a tool.
We fully agree that the local quality of both antenatal and postnatal screening significantly affects the measured benefit of pulsatility index. Several articles draw the distinction here between ‘tertiary’ and ‘non-tertiary’ units, though it may be more accurate to distinguish ‘better resourced’ from ‘less resourced’ settings, particularly in relation to antenatal scanning. As described in our original article, the apparent potential of PI screening in ‘less resourced’ settings seems strong, especially since many pulse oximetry sensors already measure it. Both Schena et al (2017) and Granelli & Ostman-Smith (2007) highlight a small but important population of babies not detected by standard screening, but with abnormal pre-morbid pulsatility indices. It seems incongruous, however, to extrapolate a single extra case detected by th...
Show MoreThe review by Searle et al “Does pulsatility index add value to newborn pulse oximetry screening for critical congenital heart disease?" (Searle 2018), provides a comprehensive overview of the current evidence regarding the addition of perfusion index to the CCHD screening algorithm.
Show MoreThe authors’ main concern is that adding pulsatility index (perfusion index, PI) will not significantly improve the current detection rate which is already quite high. As a proof, they cite the work of the large trial by Schena et al, (Schena 2017) that found one additional case of CCHD in 42,169 babies examined. The authors conclude that incorporating PI into current screening algorithms provides little additional benefit in detecting CCHD and confers a high false positive rate.
We would like to voice several comments regarding this article:
First, in the study of Schena et al, CCHD was suspected before screening in 36/38 cases in tertiary centers. This is the main reason that PI (and pulse oximetry screening) did not have any additional value in tertiary centers. In this study, only 23.6% of the neonates were born in non-tertiary center. We suggest that an alternative way to describe the results is that in non-tertiary centers, pulse oximetry detected 2 cases and PI detected an additional 1 case per approximately 10,000 screened neonates. Therefore, adding PI to the screening algorithm improved the detection rate by 50%. Moreover, the 2 cases detected by pulse oximetry...
Seo et al. conducted a prospective study to identify factors for cardiovascular disease risk factor clustering (CVD-RFC) in adolescents (1). A total of 1309 children aged 6-15 years were enrolled, and higher household income was a significant predictor of lower CVD-RFC incidence with dose-response relationship. In contrast, the presence of parental CVD history, overweight or obesity, and shorter sleep duration were significant predictors of higher CVD-RFC incidence. I have some comments with special reference to socioeconomic status (SES) and metabolic components.
First, Iguacel et al. investigated the association between socioeconomic disadvantages and metabolic syndrome (MetS) in children (2). By adjusting diet, physical activity, sedentary behaviours and well-being, standardized multiple regression coefficients (99% confidence intervals [CI]) of children from low-income families, non-traditional families, with parents of unemployment, and accumulation of >3 socioeconomic disadvantages for a higher MetS score were 0.20 (0.03-0.37), 0.14 (0.02-0.26), 0.31 (0.05-0.57), 0.21 (0.04-0.37), respectively. These data present that low SES was closely associated with MetS in children, which was in concordance with data by Seo et al (1).
Second, Patel et al. examined the association between parental socioeconomic position (SEP) and early-life offspring body mass index (BMI) in children (3). Adjusted difference of BMI z-score (95% CI) was 0.08 (0-0.16) among girls...
Show MoreDear Sir,
It is with great interest that we read ‘Why do babies cry?” in which Dr. Robert Scott-Jupp have provided a concise evaluation of the research pertaining to non-pathologic crying in infants.
Crying is a normal variant in the day 2 newborn examination however it can pose a significant source of stress and anxiety for parents. To add to the body of evidence detailed in this article we posed the question; What proportion of babies cry during the day 2 newborn examination?
A convenience sample of data was collected on well babies during the standard day 2 physical examination on the postnatal ward in a tertiary maternity hospital. All babies on the postnatal ward were eligible for inclusion. Gestation, birth weight, gender, mode of delivery and duration of examination were recorded. The presence or absence of crying during examination was documented. The data was analysed using SPSS .
One hundred and fifty three babies (n=153) were included in the study. There were 82 male infants (53%) and 71 female infants (47%). Mean birth weight was 3589g (range 2590g -5160g) with a mean gestation of 39+4 (Range 36+3 - 42+1). Mean duration of examination was 7 minutes. Eighty-one babies (52.9%) delivered by spontaneous vaginal delivery, 22 (14.4%) by ventouse, 26 (16.9%) by elective caesarean section, 20 (13.1%) by emergency caesarean section and 4(2.6%) by forceps. Overall, 118 (77.1%) babies were observed to cry during the physical examination (78%...
Show MoreDear Sir,
As a final year medical student, I read with great interest this article highlighting the pedagogical value of gaze study. Whilst the article raises many poignant features of this new medium of data collection, I believe the definition of saccade in your article may be slightly incomplete.
The article states that “Saccades...are movements of the eyes between fixations in which information is not meaningfully acquired or absorbed.” However, I would suggest that whilst the primary purpose of saccades may be to move between fixation points, there is subconscious information acquisition completed by these movements-- the subconscious identification of a lack of pathology.
If one does not take certain regions of an image as fixation points, it suggests that they are not looking for pathology in those regions. This is reinforced by one study analysing gaze study in mammogram analysis which reported that “long saccades often missed the target but were followed by corrective saccades”. (1-Kundel H, Nodine C, Conant E et al. Holistic component of image perception in mammogram interpretation: gaze-tracking study. Radiology 2007;242(2):396-402.) This highlights that within a saccade is also inert analysis of a lack of pathology rather than just transformational eye movement.
Show MoreAnother study analysing a gaze study of virtual histopathology slides between trained pathologists, residents and medical students reported that “fully trained pathologists h...
Dear Sir
We thank Professor Marchetti for his comments on our article in ADC (1). He raises two important questions we wish to comment on.
Regarding which dose of aspirin to use, we are also interested in the suggestion that anti-aggregant doses of aspirin might be a preferred option for the acute inflammatory phase of Kawasaki disease (KD). It is indeed possible that future guidance may recommend low dose aspirin (3-5 mg/kg/day) at all stages of KD, as suggested by the retrospective data referred to by Professor Marchetti (2). Whilst we acknowledge the potential merits of such an approach, particularly in relation to avoidance of toxicity, there has never been a prospective controlled clinical trial to support this and therefore no high-level evidence on which to base firm guidance. Two other practical considerations are worthy of highlighting in relation to aspirin. Firstly, nonsteroidal anti-inflammatory drugs such as ibuprofen, which antagonize platelet inhibition induced by aspirin (3), should be avoided in patients with KD receiving anti-aggregant doses of aspirin. Secondly, although the risk of low dose aspirin (3-5 mg/kg) in being associated with Reye syndrome is unknown, usual advice is to discontinue in the event of inter-current infection.
Regarding the use of corticosteroids for primary treatment of KD, we have been strong advocates of this for several years, as reflected in previously published guidance (4, 5). This is now brought into...
Show MoreDear Editor,
We thank you for the opportunity to discuss our data with the two correspondents who raised some concerns regarding the selected population of our analysis on neonatal outcomes following new reimbursement criteria on palivizumab use. They also reported data collected during the same time period and apparently different from our main results.
In response to the first correspondent, our analysis is based on children < 2 years of age because the candidate for palivizumab treatments are included within this subpopulation. In fact, the therapeutic indication (1) of palivizumab includes not only the preterm infants up to 1 year of age but also children up to 2 years of age and treated for bronchopulmonary dysplasia or born with a serious heart disease. Furthermore, our selected population is consistent with previous analysis (2) that measured the association between updated guidelines-based palivizumab administration and hospitalization for Respiratory Syncytial Virus (RSV). Table 1 of our study reports children up to 6 months of age, both at risk of RSV and including hospitalization data. We agree that this is probably the subpopulation with the major impact of the palivizumab treatment and regulatory decision. However, also in this case no differences in hospitalization rate have been detected before-after the AIFA’ limitation for palivizumab: 1031/47.608 (21.7 ‰) and 436/22715 (19.2 ‰) hospitalizations, respectiv...
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