There was an enquiry as
I immediately saw the relevance of the service provided. Only one phrase seemed to me to be discordant. "...whether a cardiac pacemaker could
be turned off during withdrawal of care, profoundly disturbing from the perspective of the clinicians.' this language , withdrawal of care is inaccurate and unfortunate. We may withdraw interventions, but not care. If the child dies as a consequence of the withdrawal I hope we care for the child during the process of dying, and look after the body with respect after the death. I hope we look after parents and siblings during the process of discussing treatment options and withdrawing. I speculate that a strong reassurance that we will continue to provide care for the child and family may be helpful in discussing withdrawing intervention.
Most of the results in table 3 express the difference as high flow minus low flow except for two in the section "VWS (hours) at 6 and 12 hours "that use low flow minus high flow.
In the abstract the primary outcome is expressed as low flow minus high flow while in Table 3 it is expressed as high flow minus low flow.
This is an underpowered study and rather than say "we find no measurably clinically relevant benefit in the use of HF compared with LF in hypoxic children......" would it be more accurate to say "we conclude there is insufficient evidence to show a difference in HF versus LF....", ie. this is called a Type 2 error.
I am sure many readers will support Chapman et al’s call to action around the need for greater confidence with, and involvement in, the treatment of very low weight eating-disordered states by paediatricians on paediatric wards. Since the article’s publication, many eating disorders resources have been made available, free of charge, which should help with this upskilling project.
However, if increasing paediatrician skill and confidence is to translate into greater acceptance of the presence of this group of young people on paediatric wards, the whole hospital paediatric workforce will need to feel more comfortable with treating very low weight eating-restriction. I am thinking here of the nurses and healthcare assistants who spend so much more time with this group of inpatients. And I am also thinking of the ward dietician.
As Chapman et al note, paediatricians have a vital role with psycho-education, in regularly reviewing the child or young person’s physical state, and in making treatment decisions based on this. However, they do not spend sustained periods of time each day at the bedside. They do not have to tolerate - for such long periods - the powerful emotional ‘projections’ that accompany each mealtime or each ng insertion ie the spoken-aloud emotional statements, as well as the belly ‘vibes’ (feelings) that one person can generate in another. It is this aspect of the daily care of children and young people in dangerous states of eating-disordered...
I am sure many readers will support Chapman et al’s call to action around the need for greater confidence with, and involvement in, the treatment of very low weight eating-disordered states by paediatricians on paediatric wards. Since the article’s publication, many eating disorders resources have been made available, free of charge, which should help with this upskilling project.
However, if increasing paediatrician skill and confidence is to translate into greater acceptance of the presence of this group of young people on paediatric wards, the whole hospital paediatric workforce will need to feel more comfortable with treating very low weight eating-restriction. I am thinking here of the nurses and healthcare assistants who spend so much more time with this group of inpatients. And I am also thinking of the ward dietician.
As Chapman et al note, paediatricians have a vital role with psycho-education, in regularly reviewing the child or young person’s physical state, and in making treatment decisions based on this. However, they do not spend sustained periods of time each day at the bedside. They do not have to tolerate - for such long periods - the powerful emotional ‘projections’ that accompany each mealtime or each ng insertion ie the spoken-aloud emotional statements, as well as the belly ‘vibes’ (feelings) that one person can generate in another. It is this aspect of the daily care of children and young people in dangerous states of eating-disordered extreme malnutrition that takes a huge emotional toll on staff, and in some hospitals has been the reason some healthcare staff cite as their reason for leaving a particular paediatric ward post.
Building skill and confidence in understanding the treatment approaches used in inpatient anorexia care is clearly key for all paediatric staff; the treatment approach can often feel a lot less collaborative than most paediatric scenarios warrant and staff may worry about being “mean” or a “bully”.
Central, therefore, is reframing the nursing approaches as being entirely the same ones that are used with any other high dependency patient ie accurately recording input and output, being firm about taking necessary medicines ( in this case calories), even when, as is so often the case during cancer treatments, a child might be refusing/ not wanting to accept the intervention that needs to happen. Being able to stay in touch with the fact that they are delivering care that is in the child’s best interests, even when the child is vocal in stating their aversion to this intervention, is hard. And this is where some kind of regular group supervision for staff is so important.
Skills and knowledge are necessary to delivering effective care for this group of children and young people, but if wards are to embrace this work in a manner that does not create toxic effects in staff, either in terms of unhelpful attitudes towards eating-disordered patients, or in terms of staff burn out, the emotional impact of the tasks involved must be factored into the day-to-day running of the ward.
Dr Virginia Davies
MRCP FRCPsych MRCGP
Consultant in paediatric liaison
Paediatric mental health team
Whittington Hospital
Varghese and colleagues draw attention to and argue for better capture of the link between air pollution and fatal or near-fatal asthma at a patient level [1]
Evidence on the detrimental effects of air pollution on health have led to the World Health Organisation proposing stringent targets in guidelines for improving air quality [2,3], which in the UK we fall far short of [4].
There is a clear mismatch: if air pollution is a major risk for 5 million excess deaths per year globally and 30-40 thousand excess deaths in the UK [5], why is that risk rarely discussed in clinical consultations or documented in clinical records? We frequently ask about smoking and pets in the household when taking a clinical history, but not about outdoor air pollution exposure in terms of where children live or how they walk to school in relation to local busy roads.
In 2020 the result of an inquest linked the death of a 9 year old girl, to air pollution based on careful examination of timing of admissions and spikes in air pollution over the preceding years. The coroner rightly criticised many professional groups. This included those responsible for medical education for failing to focus on air pollution and clinicians for failing to warn this girl’s family about the health risks of air pollution [6].
So despite the considerable scientific evidence, air pollution is seldom recorded clinically. It has a code that is rarely used (Exposure to air pollution ICD10 Co...
Varghese and colleagues draw attention to and argue for better capture of the link between air pollution and fatal or near-fatal asthma at a patient level [1]
Evidence on the detrimental effects of air pollution on health have led to the World Health Organisation proposing stringent targets in guidelines for improving air quality [2,3], which in the UK we fall far short of [4].
There is a clear mismatch: if air pollution is a major risk for 5 million excess deaths per year globally and 30-40 thousand excess deaths in the UK [5], why is that risk rarely discussed in clinical consultations or documented in clinical records? We frequently ask about smoking and pets in the household when taking a clinical history, but not about outdoor air pollution exposure in terms of where children live or how they walk to school in relation to local busy roads.
In 2020 the result of an inquest linked the death of a 9 year old girl, to air pollution based on careful examination of timing of admissions and spikes in air pollution over the preceding years. The coroner rightly criticised many professional groups. This included those responsible for medical education for failing to focus on air pollution and clinicians for failing to warn this girl’s family about the health risks of air pollution [6].
So despite the considerable scientific evidence, air pollution is seldom recorded clinically. It has a code that is rarely used (Exposure to air pollution ICD10 Code Z58.1) and is not being listed as a contributing factor on the medical certificates of death [7]. As Smith et al point out there is government advice on when to include “smoking, alcohol and occupational exposures on death certificates but not when to include air pollution” [7].
Does it matter, and do we clinicians have a role in this?
Clearly the answer has to be yes – if we are not even trying to access information on air pollution at a time of hospital admission how can we begin to discuss it? Clinicians are busy and traditionally have received little in their education about the health effects of air pollution.
One way of alerting and educating clinical staff to a patient’s potential exposure is by automating information relating air quality to home postcode in electronic clinical records. This has been done at Great Ormond Street Hospital NHS Foundation Trust, Guys’ and St Thomas’ NHS Foundation Trust and King’s College Hospital NHS Foundation Trust when a patient lives in an area with levels above the WHO 2021 recommendations [8]. Not only does this alert the clinician to the relevant air quality data for that patient but “hover bubbles” provide an educational component and can be used for communication with primary care and the patient/family. Data collected and appropriately coded may be used for future much needed monitoring and research.
We would argue that air pollution is such an important health issue with effects across the lifespan, that we have a professional responsibility to speak widely about it. Without systems to help educate clinicians, inform patient management, and describe individual adverse clinical outcomes more accurately including in communications, we risk air pollution being continued to be overlooked as an important cause of ill health and death. We also lose the authority to demand infrastructure and policy changes required to clean the air we all breathe.
Yours sincerely,
Dr Heather J Lambert, Paediatrician and Research Associate, University of Newcastle upon Tyne
Dr Mark J Hayden, Consultant Paediatric Intensivist, Great Ormond Street Hospital NHS Foundation Trust
Dr Chinthika Piyasena, Consultant Neonatologist, Guys’ and St Thomas’ NHS Foundation Trust
Dr Stephen W Lord , Consultant Cardiologist and Medical Examiner
Newcastle upon Tyne Hospitals NHS Foundation Trust and Chair Medical Education Leaders UK
References
1. Varghese D, Clemens T, McMurray A, et al. Near-fatal and fatal asthma and air pollution: are we missing an opportunity to ask key questions?
Arch Dis Child Epub ahead of print: Oct 2023. doi:10.1136/archdischild-2023-325548
2. Taylor L. WHO cuts air pollution limits to save millions of lives. BMJ 2021;374:n2349.
3. WHO global air quality guidelines: particulate matter (PM2.5 and PM10), ozone, nitrogen dioxide, sulfur dioxide and carbon monoxide. 21 Sep 2021. ISBN 9789240034228.
7. Smith LJ, Tomson M, Brown K. Air pollution should be listed on death certificates. BMJ 2023;383:2162.
8. Hayden M, Andersson J, Wilson N, Fecht D. Taking air pollution to the next level – displaying in the patients chart and empowering action. Archives of Disease in Childhood 2023;108:A291-A292.
The importance of objective assessment of prenatal exposure to alcohol through measurement of biomarkers in meconium
Oscar Garcia-Algar1,2,3*, Luigi Tarani4, Francesco Paolo Busardò5, Simona Pichini3,5, Emilia Marchei5
1. Neonatology Unit, Hospital Clinic-Maternitat, ICGON, BCNatal, Barcelona Centre for Maternal Foetal and Neonatal Medicine, Hospital Sant Joan de Déu and Hospital Clínic, Barcelona, Spain
2. Department de Cirurgia i Especialitats Mèdico-Quirúrgiques, Universitat de Barcelona, Barcelona, Spain
3. European Foetal Alcohol Spectrum Disorders Alliance (EUFASD), Stockholm, Sweden
4. Department of Pediatrics, Sapienza University of Rome, Rome, Italy
5. National Centre on Addiction and Doping, Istituto Superiore di Sanità, Rome, Italy
Dear Editor,
We read with attention the paper by Henderson et al. concerning comparison of confidential postnatal maternal interview and measurement of alcohol biomarkers in meconium (1). We would like to draw attention on their conclusion: “Fatty acid ethyl esters (FAEEs) and Ethylglucuronide (EtG) measured in meconium have low sensitivity and specificity for self-reported alcohol consumption after 20 weeks’ gestation in an unselected Scottish population and measurement of these alcohol biomarkers in meconium cannot currently be recommended for the identification of newborns at risk of Fetal Alcohol Spectrum Disorders (FASD).”
It has been more than 20 years since meconium analy...
The importance of objective assessment of prenatal exposure to alcohol through measurement of biomarkers in meconium
Oscar Garcia-Algar1,2,3*, Luigi Tarani4, Francesco Paolo Busardò5, Simona Pichini3,5, Emilia Marchei5
1. Neonatology Unit, Hospital Clinic-Maternitat, ICGON, BCNatal, Barcelona Centre for Maternal Foetal and Neonatal Medicine, Hospital Sant Joan de Déu and Hospital Clínic, Barcelona, Spain
2. Department de Cirurgia i Especialitats Mèdico-Quirúrgiques, Universitat de Barcelona, Barcelona, Spain
3. European Foetal Alcohol Spectrum Disorders Alliance (EUFASD), Stockholm, Sweden
4. Department of Pediatrics, Sapienza University of Rome, Rome, Italy
5. National Centre on Addiction and Doping, Istituto Superiore di Sanità, Rome, Italy
Dear Editor,
We read with attention the paper by Henderson et al. concerning comparison of confidential postnatal maternal interview and measurement of alcohol biomarkers in meconium (1). We would like to draw attention on their conclusion: “Fatty acid ethyl esters (FAEEs) and Ethylglucuronide (EtG) measured in meconium have low sensitivity and specificity for self-reported alcohol consumption after 20 weeks’ gestation in an unselected Scottish population and measurement of these alcohol biomarkers in meconium cannot currently be recommended for the identification of newborns at risk of Fetal Alcohol Spectrum Disorders (FASD).”
It has been more than 20 years since meconium analysis has been used to objectively assess prenatal exposure to alcohol (2-12). Several studies have been reported in the literature regarding the use of this biological matrix for the determination of alcohol biomarkers such as FAEEs and EtG and to be used in epidemiological studies verifying alcohol drinking during pregnancy and consequentially prenatal exposure. These studies not only assessed prenatal exposure to gestational alcohol, but also demonstrated underreporting and misreporting of pregnant women concerning gestational drinking habits. To this concern, the majority of studies from our group showed no relationship between biomarker measurement and maternal self-reported declarations, at least in the Mediterranean area where investigations were carried out (13-26).
In this paper, an anonymised, observational population-based study questionnaire on alcohol consumption in pregnancy was matched with measurement of alcohol biomarkers in meconium in a cohort of mother/infant dyads from Glasgow, UK. Of 828 women enrolled in the study, 384 (46.4%) reported alcohol consumption at any time in pregnancy and for 114 (13.6%) this was after 20 weeks’ gestation. When meconium was positive for FAEEs (≥ 600 ng/g) and for EtG (≥ 30 ng/g), 14.5% and 10.7% of mothers reported alcohol consumption after 20 weeks’ gestation, respectively. Similar percentages were observed when meconium was negative for FAEEs (13.0%, ≤ 600 ng/g) and for EtG (14.0%, ≤ 30 ng/g). The authors concluded that FAEE and EtG measured in meconium showed low sensitivity and specificity for self-reported alcohol consumption after 20 weeks of gestation.
Based on the determination of biomarkers, FAEEs were identified in all meconium samples analyzed and 39.6% had a concentration greater than or equal to 600 ng/mg (cut-off used to discriminate positive from negative samples). As far as EtG is concerned, 14.5% of the analyzed meconium samples had a concentration greater than or equal to 30 ng/g (cut-off used to discriminate positive samples from negative ones). In summary, if the biomarkers are also considered, the percentage of potentially exposed children increases, therefore it is possible to intervene also on those who, from the questionnaire, would have appeared to be newborns of non-drinking women and therefore excluded from any follow-up.
Early diagnosis of foetal alcohol spectrum disorders is of crucial importance to perform a targeted follow up of newborns prenatally exposed to alcohol and avoid secondary neurodevelopmental disabilities. A positive meconium testing for the presence of EtG or FAEEs is an objective first element to assess prenatal exposure to alcohol, whereas a maternal self-reported admission of gestational consumption of alcohol is not.
The only use of self-reported questionnaires to disclose alcohol drinking during pregnancy can’t be recommended. In addition, we do not have to forget transplacental passage of this teratogen, which differs in each mother-infant dyad and can either allow or prevent alcohol migration from the mother to the foetus.
In conclusion, we reiterate the importance of objective assessment of gestational drinking and consequent foetal exposure by measuring alcohol metabolites not only in neonatal meconium, but also in maternal hair to associate the results of these measurements to a potential brief intervention on the risks of gestational alcohol to mothers and neurodevelopmental targeted follow up for exposed newborns (18, 26).
References
1. Henderson EM, Tappin D, Young D, et al Assessing maternal alcohol consumption in pregnancy: comparison of confidential postnatal maternal interview and measurement of alcohol biomarkers in meconium. Arch. Dis. Child. 2023, 2022-325028.
2. Bearer CF, Lee S, Salvator AE, et al. Ethyl linoleate in meconium: a biomarker for prenatal ethanol exposure. Alcohol Clin Exp Res. 1999, 23, 487-493.
3. Klein J, Karaskov T, Korent G. Fatty acid ethyl esters: a novel biologic marker for heavy in utero ethanol exposure: a case report. Ther Drug Monit. 1999, 21, 644-646.
4. Ostrea EM Jr, Hernandez JD, Bielawski DM et al. Fatty acid ethyl esters in meconium: are they biomarkers of fetal alcohol exposure and effect? Alcohol Clin Exp Res. 2006, 30, 1152-1159.
5. Gareri J, Lynn H, Handley M, et al.. Prevalence of fetal ethanol exposure in a regional population-based sample by meconium analysis of fatty acid ethyl esters. Ther Drug Monit. 2008, 30, 239-245.
6. Pichini S, Pellegrini M, Gareri J, et al. Liquid chromatography-tandem mass spectrometry for fatty acid ethyl esters in meconium: assessment of prenatal exposure to alcohol in two European cohorts. J Pharm Biomed Anal. 2008, 48, 927-933.
7. Morini L, Marchei E, Pellegrini M, et al. Liquid chromatography with tandem mass spectrometric detection for the measurement of ethyl glucuronide and ethyl sulfate in meconium: new biomarkers of gestational ethanol exposure? Ther Drug Monit. 2008, 30, 725-732.
8. Pichini S, Morini L, Marchei E, et al. Ethylglucuronide and ethylsulfate in meconium to assess gestational ethanol exposure: preliminary results in two Mediterranean cohorts. Can J Clin Pharmacol. 2009, 16, e370-e375.
9. Hastedt M, Krumbiegel F, Gapert R, et al. Fatty acid ethyl esters (FAEEs) as markers for alcohol in meconium: method validation and implementation of a screening program for prenatal drug exposure. Forensic Sci Med Pathol. 2013, 9, 287-295.
10. Pichini S, Morini L, Pacifici R, et al. Development of a new immunoassay for the detection of ethyl glucuronide (EtG) in meconium: validation with authentic specimens analyzed using LC-MS/MS. Preliminary results. Clin Chem Lab Med. 2014, 52, 1179-1185.
11. Abernethy C, McCall KE, Cooper G, et al. Determining the pattern and prevalence of alcohol consumption in pregnancy by measuring biomarkers in meconium. Arch Dis Child Fetal Neonatal Ed. 2018, 103, F216-F220.
12. Woźniak MK, Banaszkiewicz L, Aszyk J, et al. Development and validation of a method for the simultaneous analysis of fatty acid ethyl esters, ethyl sulfate and ethyl glucuronide in neonatal meconium: application in two cases of alcohol consumption during pregnancy. Anal Bioanal Chem. 2021, 413, 3093-3105.
13. Derauf C, Katz AR, Easa D. Agreement between maternal self-reported ethanol intake and tobacco use during pregnancy and meconium assays for fatty acid ethyl esters and cotinine. Am J Epidemiol. 2003, 158, 705-709.
14. Garcia-Algar O, Kulaga V, Gareri J, et al. Alarming prevalence of fetal alcohol exposure in a Mediterranean city. Ther Drug Monit. 2008, 30, 249-254.
15. Pichini S, Garcia-Algar O, Klein J, et al. FAEEs in meconium as biomarkers of maternal drinking habit during pregnancy. Birth Defects Res A Clin Mol Teratol. 2009, 85, 230; author reply 231-232.
16. Bakhireva LN, Savage DD. Focus on: biomarkers of fetal alcohol exposure and fetal alcohol effects. Alcohol Res Health. 2011, 34, 56–63.
17. Zelner I, Shor S, Lynn H, et al. Clinical use of meconium fatty acid ethyl esters for identifying children at risk for alcohol-related disabilities: the first reported case. J Popul Ther Clin Pharmacol. 2012, 19, e26-31.
18. Pichini S, Marchei E, Vagnarelli F, et al. Assessment of prenatal exposure to ethanol by meconium analysis: results of an Italian multicenter study. Alcohol Clin Exp Res. 2012, 36, 417-424.
19. Manich A, Velasco M, Joya X, et al. Validez del cuestionario de consumo materno de alcohol para detectar la exposición prenatal [Validity of a maternal alcohol consumption questionnaire in detecting prenatal exposure]. An Pediatr (Barc). 2012, 76, 324-328.
20. Memo L, Gnoato E, Caminiti S, et al. Fetal alcohol spectrum disorders and fetal alcohol syndrome: the state of the art and new diagnostic tools. Early Hum Dev. 2013, 89, S40-3.
21. Joya X, Marchei E, Salat-Batlle J, et al. Fetal exposure to ethanol: relationship between ethyl glucuronide in maternal hair during pregnancy and ethyl glucuronide in neonatal meconium. Clin Chem Lab Med. 2016, 54, 427-435.
22. Chiandetti A, Hernandez G, Mercadal-Hally M, et al. Prevalence of prenatal exposure to substances of abuse: questionnaire versus biomarkers. Reprod Health. 2017, 14, 137.
23. Gomez-Roig MD, Marchei E, Sabra S, et al. Maternal hair testing to disclose self-misreporting in drinking and smoking behavior during pregnancy. Alcohol. 2018, 67, 1-6.
24. Min MO, Minnes S, Momotaz H, et al. Fatty acid ethyl esters in meconium and substance use in adolescence. Neurotoxicol Teratol. 2021, 83,106946.
25. Maschke J, Roetner J, Goecke TW, et al. Prenatal Alcohol Exposure and the Facial Phenotype in Adolescents: A Study Based on Meconium Ethyl Glucuronide. Brain Sci. 2021, 11, 154.
26. La Maida N, Di Giorgi A, Pellegrini M, et al. Reduced prevalence of fetal exposure to alcohol in Italy: a nationwide survey. Am J Obstet Gynecol MFM. 2023, 25:100944.
Many thanks for an important study. It raises the question if a distinction between Reactive Attachment Disorder and autism based on the presumed aetiology can be sustained. The genetic aetiology of autism spectrum conditions was established on the impressive difference in concordance rates between MZ and DZ twins but there are epigenetic mechanisms which could explain this difference. MZ twins have exactly equal biochemical exposures before conception (preconception environment) whereas DZ twins do not. A number of environmental exposures in prior generations are associated with autism (Magdelena 2020, Golding 2021). A huge study of the MSSNG database finds a genetic cause involving different 134 genes in only 14% of autistic individuals (Trost 2023). What then is being acquired or inherited? If the answer is early childhood stress, the rise in autism need not be spurious.
Great work Nicki. I have long argued the need for more paediatric respirologists to service this expanding population. There is a shortage of pediatric pulmonologists [sic] in the USA and most in practice are graying. Now we have data to support this argument. Of greater concern is the (lack of) availability of home nursing support, placing tremendous stress on family. In part due to the “mass resignation” arising during and after the pandemic, there is critical shortage of trained personnel to care for such children in their homes. We have been forced to start weaning patients from mechanical ventilatory support – chiefly those with chronic lung disease of prematurity – while they are still hospitalized before initial NICU discharge. Indeed, we may have our first decannulation of one such child in the next few months! Thank you for undertaking this study and reporting the trend we all foresaw.
Pubertal staging is rarely needed in a general paediatric clinic and I wonder if there is a way to avoid the difficult issues in examining older children and young people.
I think the issues around chaperones are complex, as a male doctor, male patients often do not want a female nurse as a chaperone and on the whole peri-pubertal girls do not want to be examined at all by a male doctor.
My strategy, when needed, is therefore to ask older children and young people to let me know what they think their pubertal stage is - testicular size can be self-assessed using a standard orchidometer, all other changes can be described with reference to standard drawings from a growth chart.
I realise this is not evidence based practice but wonder if there is the possibility of a trial to compare paediatrician-assessed as opposed to self-assessed staging in non-specialist clinics?
Dear authors, the article made for some interesting reading especially as the current DKA ICP recommended by BSPED has now been in force for almost 2 years. It provides some perspective on whether the difference in liberalized vs conservative management is clinically significant or otherwise. Our question relates to whether the authors found any data in the studies regarding change in osmolarity / rate of rise of sodium which are early predictors for risk of cerebral oedema.
There was an enquiry as
I immediately saw the relevance of the service provided. Only one phrase seemed to me to be discordant. "...whether a cardiac pacemaker could
be turned off during withdrawal of care, profoundly disturbing from the perspective of the clinicians.' this language , withdrawal of care is inaccurate and unfortunate. We may withdraw interventions, but not care. If the child dies as a consequence of the withdrawal I hope we care for the child during the process of dying, and look after the body with respect after the death. I hope we look after parents and siblings during the process of discussing treatment options and withdrawing. I speculate that a strong reassurance that we will continue to provide care for the child and family may be helpful in discussing withdrawing intervention.
Most of the results in table 3 express the difference as high flow minus low flow except for two in the section "VWS (hours) at 6 and 12 hours "that use low flow minus high flow.
In the abstract the primary outcome is expressed as low flow minus high flow while in Table 3 it is expressed as high flow minus low flow.
This is an underpowered study and rather than say "we find no measurably clinically relevant benefit in the use of HF compared with LF in hypoxic children......" would it be more accurate to say "we conclude there is insufficient evidence to show a difference in HF versus LF....", ie. this is called a Type 2 error.
"Nineteen per cent of reported cases had an elevated ASOT (200 IU/mL or above) and the mean titre was 600 IU/mL. "
Is 600 the mean of all ASOT measured, or just the 19% of children with elevated results?
I am sure many readers will support Chapman et al’s call to action around the need for greater confidence with, and involvement in, the treatment of very low weight eating-disordered states by paediatricians on paediatric wards. Since the article’s publication, many eating disorders resources have been made available, free of charge, which should help with this upskilling project.
However, if increasing paediatrician skill and confidence is to translate into greater acceptance of the presence of this group of young people on paediatric wards, the whole hospital paediatric workforce will need to feel more comfortable with treating very low weight eating-restriction. I am thinking here of the nurses and healthcare assistants who spend so much more time with this group of inpatients. And I am also thinking of the ward dietician.
As Chapman et al note, paediatricians have a vital role with psycho-education, in regularly reviewing the child or young person’s physical state, and in making treatment decisions based on this. However, they do not spend sustained periods of time each day at the bedside. They do not have to tolerate - for such long periods - the powerful emotional ‘projections’ that accompany each mealtime or each ng insertion ie the spoken-aloud emotional statements, as well as the belly ‘vibes’ (feelings) that one person can generate in another. It is this aspect of the daily care of children and young people in dangerous states of eating-disordered...
Show MoreVarghese and colleagues draw attention to and argue for better capture of the link between air pollution and fatal or near-fatal asthma at a patient level [1]
Evidence on the detrimental effects of air pollution on health have led to the World Health Organisation proposing stringent targets in guidelines for improving air quality [2,3], which in the UK we fall far short of [4].
There is a clear mismatch: if air pollution is a major risk for 5 million excess deaths per year globally and 30-40 thousand excess deaths in the UK [5], why is that risk rarely discussed in clinical consultations or documented in clinical records? We frequently ask about smoking and pets in the household when taking a clinical history, but not about outdoor air pollution exposure in terms of where children live or how they walk to school in relation to local busy roads.
In 2020 the result of an inquest linked the death of a 9 year old girl, to air pollution based on careful examination of timing of admissions and spikes in air pollution over the preceding years. The coroner rightly criticised many professional groups. This included those responsible for medical education for failing to focus on air pollution and clinicians for failing to warn this girl’s family about the health risks of air pollution [6].
So despite the considerable scientific evidence, air pollution is seldom recorded clinically. It has a code that is rarely used (Exposure to air pollution ICD10 Co...
Show MoreThe importance of objective assessment of prenatal exposure to alcohol through measurement of biomarkers in meconium
Oscar Garcia-Algar1,2,3*, Luigi Tarani4, Francesco Paolo Busardò5, Simona Pichini3,5, Emilia Marchei5
1. Neonatology Unit, Hospital Clinic-Maternitat, ICGON, BCNatal, Barcelona Centre for Maternal Foetal and Neonatal Medicine, Hospital Sant Joan de Déu and Hospital Clínic, Barcelona, Spain
2. Department de Cirurgia i Especialitats Mèdico-Quirúrgiques, Universitat de Barcelona, Barcelona, Spain
3. European Foetal Alcohol Spectrum Disorders Alliance (EUFASD), Stockholm, Sweden
4. Department of Pediatrics, Sapienza University of Rome, Rome, Italy
5. National Centre on Addiction and Doping, Istituto Superiore di Sanità, Rome, Italy
Dear Editor,
Show MoreWe read with attention the paper by Henderson et al. concerning comparison of confidential postnatal maternal interview and measurement of alcohol biomarkers in meconium (1). We would like to draw attention on their conclusion: “Fatty acid ethyl esters (FAEEs) and Ethylglucuronide (EtG) measured in meconium have low sensitivity and specificity for self-reported alcohol consumption after 20 weeks’ gestation in an unselected Scottish population and measurement of these alcohol biomarkers in meconium cannot currently be recommended for the identification of newborns at risk of Fetal Alcohol Spectrum Disorders (FASD).”
It has been more than 20 years since meconium analy...
Many thanks for an important study. It raises the question if a distinction between Reactive Attachment Disorder and autism based on the presumed aetiology can be sustained. The genetic aetiology of autism spectrum conditions was established on the impressive difference in concordance rates between MZ and DZ twins but there are epigenetic mechanisms which could explain this difference. MZ twins have exactly equal biochemical exposures before conception (preconception environment) whereas DZ twins do not. A number of environmental exposures in prior generations are associated with autism (Magdelena 2020, Golding 2021). A huge study of the MSSNG database finds a genetic cause involving different 134 genes in only 14% of autistic individuals (Trost 2023). What then is being acquired or inherited? If the answer is early childhood stress, the rise in autism need not be spurious.
Great work Nicki. I have long argued the need for more paediatric respirologists to service this expanding population. There is a shortage of pediatric pulmonologists [sic] in the USA and most in practice are graying. Now we have data to support this argument. Of greater concern is the (lack of) availability of home nursing support, placing tremendous stress on family. In part due to the “mass resignation” arising during and after the pandemic, there is critical shortage of trained personnel to care for such children in their homes. We have been forced to start weaning patients from mechanical ventilatory support – chiefly those with chronic lung disease of prematurity – while they are still hospitalized before initial NICU discharge. Indeed, we may have our first decannulation of one such child in the next few months! Thank you for undertaking this study and reporting the trend we all foresaw.
Pubertal staging is rarely needed in a general paediatric clinic and I wonder if there is a way to avoid the difficult issues in examining older children and young people.
I think the issues around chaperones are complex, as a male doctor, male patients often do not want a female nurse as a chaperone and on the whole peri-pubertal girls do not want to be examined at all by a male doctor.
My strategy, when needed, is therefore to ask older children and young people to let me know what they think their pubertal stage is - testicular size can be self-assessed using a standard orchidometer, all other changes can be described with reference to standard drawings from a growth chart.
I realise this is not evidence based practice but wonder if there is the possibility of a trial to compare paediatrician-assessed as opposed to self-assessed staging in non-specialist clinics?
Dear authors, the article made for some interesting reading especially as the current DKA ICP recommended by BSPED has now been in force for almost 2 years. It provides some perspective on whether the difference in liberalized vs conservative management is clinically significant or otherwise. Our question relates to whether the authors found any data in the studies regarding change in osmolarity / rate of rise of sodium which are early predictors for risk of cerebral oedema.
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