Displaying 11-20 letters out of 546 published
Re:Minimally-invasive (and painful?) surfactant therapy.
Sir, we read with interest the article by Dargaville et al., entitled "Minimally-invasive surfactant therapy in preterm infants on continuous positive airway pressure", in which the authors describe significant results using a semirigid vascular catheter inserted into the trachea by direct laringoscopy for surfactant administration, without analgesia and sedation(1). However, direct laringoscopy and tracheal manipulation, is an extremely distressing and painful procedure, with potential for airway and systemic injury. It is well established that direct laringoscopy and tracheal intubation without analgesia should be performed only for urgent resuscitations. Neonatal pain may result in altered systemic and cerebral blood pressure, intracranial hemorrhage, hypersensitive pain perception and long-term sequelaes(2). In their study 36% of the neonates had bradycardia sustained for more than 10s during laryngoscopy or vocal cord manipulation. It is now evident that initial stabilization with CPAP and rescue surfactant administration if necessary, is not worse than intubation, mechanical ventilation and surfactant administration immediately after birth. INSURE procedure is an alternative, combining early surfactant and CPAP. Welzing et al. have shown that INSURE can be performed using remifentanil as premedication for tracheal intubation with excellent neonatal outcome(3). In the same way, our group have shown that remifentanil as premedication allows early awakening and extubation(4). However, the short period of positive pressure ventilation required for INSURE, even if an ultra short acting opioid is used, could compromise the benefit of early surfactant. In this way, some reports have shown that a laryngeal mask airway (LMA) as a conduit for surfactant administration could be a simple and painless procedure(5). Trials of surfactant administration through the LMA are now being conducted. So, finding a noninvasive and painless method of surfactant administration, without laryngoscopy, tracheal manipulation and positive pressure ventilation, will be one of the most important subjects for neonatology research in upcoming years.
References 1.Dargaville PA, et al. Minimally-invasive surfactant therapy in preterm infants on continuous positive airway pressure. Arch Dis Child Fetal Neonatal Ed 2013;98:F122-F126. 2.Carbajal R, Eble B, Anand KJ. Premedication for tracheal intubation in neonates: confusion or controversy? Semin Perinatol 2007;3:309-17. 3.Welzing L, Kribs A, Huenseler C, Eifinger F, Mehler K, Roth B. Remifentanil for INSURE in preterm infants: a pilot study for evaluation of efficacy and safety aspects. Acta Paediatr 2009;98:1416-20. 4.e Silva YP, Gomez RS, Marcatto JdeO, Maximo TA, Barbosa RF, Silva AC. Early awakening and extubation with remifentanil in ventilated premature neonates. Paediatr Anaesth 2008;18:176-83. 5.Trevisanuto D, Grazzina N, Ferrarese P, Micaglio M, Verghese C, Zanardo V. Laryngeal mask airway used as a delivery conduit for the administration of surfactant to preterm infants with respiratory distress syndrome. Biol Neonate 2005;87:217-20.
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Born just a few weeks early: does it matter?
Sarah J Kotecha1, John Henderson2, Sailesh Kotecha1.
1Department of Child Health, Cardiff University, Cardiff. 2School of Social and Community Medicine, University of Bristol, Bristol.
Re: Born just a few weeks early: does it matter? Boyle et al. 98:F85- 88. Doi:10.1136/archdischild-2011-300535.
We read with interest the review by Boyle and Boyle on early and late morbidity in late preterm born children (1). Clearly there is increasing interest in late preterm born infants who have both increased short- and importantly long-term mortality and morbidity as we reviewed recently (2). Of interest to readers of Archives of Diseases of Childhood, will be recent publications using data from the Avon Longitudinal Study of Parents and Children cohort on longer term respiratory function and neurodevelopmental outcomes. Like Abe et al (3), we did not find strong evidence of an association between asthma and late preterm birth but we have reported decrements in FEV1 in late preterm infants, (born at 33-34 weeks gestation), at 8-9 years of age of the same magnitude as extremely preterm infants, (born at 25-32 weeks gestation), (4), recently highlighted in a Thorax editorial (5). Encouragingly, we did see improvements in FEV1 when the late preterm born infants were studied again at 14-17 years of age but clearly further studies are required to assess if these children are candidates for chronic pulmonary obstructive disease in adulthood especially if exposed to noxious substances such as tobacco smoke and environmental pollution. Furthermore, children born late-preterm are less likely to be successful in early school assessments than those born at term (6). In addition to those mentioned by Boyle and Boyle there is increasing literature in this field in particular reporting the longer term outcomes of this population; despite these observations, a recent survey by the British Thoracic Society of respiratory physicians noted that little consideration is given to early life factors when patients with respiratory disease are seen in their clinical practice (7). We are sure readers of Archives of Diseases of Childhood will be as concerned as we are about the potential public health impact of these effects if they are carried through the life course from 8-9 years into adulthood, especially as late preterm infants are a growing population.
1. Boyle JD, Boyle EM. Born just a few weeks early: does it matter? Arch Dis Child Fetal Neonatal Ed 2013;98:F85-88. Doi:10.1136/archdischild- 2011-300535. 2. Kotecha SJ, Dunstan FD, Kotecha S. Long term respiratory outcomes of late preterm-born infants. Semin Fetal Neonatal Med 2012 Apr;17(2):77-81. 3. Abe K, Shapiro-Mendoza CK, Hall LR, et al. Late preterm birth and risk of developing asthma. J Pediatr 2010;157:74-8. 4. Kotecha SJ, Watkins WJ, Paranjothy S, Dunstan FD, Henderson AJ, Kotecha S. Effect of late preterm birth on longitudinal lung spirometry in school age children and adolescents. Thorax 2012 Jan;67(1):54-61. 5. Bush A, Pavord ID. Thorax: the Cappuccino years. 2013 Jan;68(1): 1-4. 6. Peacock PJ, Henderson J, Odd D, Edmond A. Early school attainment in late-preterm infants. Arch Dis Child 2012;97:118-120. doi:10.1136/118 adc.2011.300925 7. Bolton CE, Bush A, Hurst JR, Kotecha S, McGarvey L, Stocks J, Walshaw M. Are Early Life Factors Considered when Managing Respiratory Disease? A British Thoracic Society (BTS) Survey of Current Practice. Thorax 2012 Dec;67(12):1110 (Research Letter)
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None to declare
Conflict of Interest: None declared
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Should air insufflation to aid location of gastric feeding tube tip location in neonates become standard practice?
Quandt et al (1) have emphasised stomach insufflation as a means to improve neonatal feeding tube location rates. Experience in our neonatal unit indicates that other measures may be more important.
It is a practice standard in our neonatal unit for a gastric tube to be placed prior to performing the first chest radiograph. We retrospectively audited all first chest radiographs taken during the six month period from August 2011 to February 2012. We excluded infants who were born in another hospital or if there was no gastric tube present on first radiograph. Eighty-eight neonates fulfilled the inclusion criteria. Images were viewed on PACS (online digital radiograph viewing system). We scored the tube position as per Quandt et al (1) and images were viewed independently by two individuals (RB and LS) and results correlated. Tube tip was locatable in 90% of radiographs with sixty-seven in the stomach and thirteen outside the stomach. Of the eight radiographs with an unlocatable tip, all were explainable by truncation of the radiograph.
In summary, we did not find that prior air insufflation would have aided location. We did however identify a requirement to specify in the radiology request that the stomach be included in the radiographic field and also that the procedure for measuring estimated gastric tube length needed to be reviewed.
1. Quandt D, Brons E, Schiffer PM, et al. Improved radiological assessment of neonatal feeding tubes. Arch Dis Child Fetal Neonatal Ed 2013;98:F78-F80.
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Delay in identification of oesophageal atresia in a preterm neonate with radial club hand due to coiling of 5F nasogastric tube
We had a 29 weeks/1.29kg/male neonate born with left radial club hand deformity. The resident attending the resuscitation had 'passed' a 5F nasogastric tube and certified the orifices patent. Baby was admitted in NICU, had no respiratory distress and was started on trophic feeds of 2ml 2 hourly by 5F nasogastric tube passed via the nostril which the baby 'accepted'. After 12 hours baby developed worsening respiratory distress and had to be ventilated. Chest X ray taken without a nasogastric tube showed right upper lobe pneumonia. With a diagnosis of aspiration pneumonia, repeat Xray with 5F tube showed its tip to be coiled upwards in the thorax and absent gastric bubble and a gasless abdomen. The diagnosis of oesophageal atresia without fistula was confirmed by a 10F tube and contrast studies. With the additional finding of vertebral segmentation defects, the baby was labelled with a diagnosis of VACTERL association. This case illustrates the need for using a large size feeding tube to rule out oesophageal atresia. Patient Consent Obtained.
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Etiology of perinatal stroke; a role for prothrombotic coagulation factors?
We read with grat interest the article on perinatal stroke of J Harteman and co-workers. In our experience in perinatal stroke, multiple, often coexisting, risk factors are involved, varying from maternal and fetal risk factors during pregnancy and delivery, to infectious causes and cardiac diseases as well as medical interventions and congenital prothrombotic coagulation factors. We have performed a retrospective study to explore the prevalence of different predisposing conditions in perinatal stroke patients we evaluated 96 patients (43 males; 53 females), including subjects with ischemic and hemorrhagic stroke subtypes. Baseline investigations included complete blood count, total cholesterol, triglycerides, lipoprotein (a), prothrombin, activated thromboplastin, plasma fibrinogen level, activity of protein C sensitivity ratio, total plasma homocysteine, lupus anticoagulant, anticardiolipin, and anti-beta2 glycoprotein1 antibodies. DNA analysis was performed for the Factor V Leiden mutation, Factor II G20219A variant, and the thermolabile variant of MTHFR. We have oberved that the major genetic risk factor in our series of patients was heterozygosity and homozigosity for the MTHFR C677T mutation (39/96 patients; 40%) in 5 patients was associated with the Factor V Leiden mutation, in 6 with deficiency of activity of protein C. Acquired predisposing conditions were present in 18/96 (18%) patients and included Threatened abortion, oligohydramnios, intra uterine growth retardation, gestosis, chorioamniositis. In 7 patients both genetic and aquired predisposing factors were present. Our results emphasize that prothrombotic coagulation risk factors, especially MTHFR mutation, can predispose to perinatal stroke, alone or in combination with other genetic or acquired factors (1,2). References 1)Muwakkit SA, Majdalani M, Hourani R, Mahfouz RA, Otrock ZK, Bilalian C, Chan AK, Abboud M, Mikati MA. Inherited thrombophilia in childhood arterial stroke: data from Lebanon.Pediatr Neurol. 2011 Sep;45(3):155-8. 2)Darmency-Stamboul V, Chantegret C, Ferdynus C, Mejean N, Durand C, Sagot P, Giroud M, Bejot Y, Gouyon JB.Antenatal factors associated with perinatal arterial ischemic stroke.Stroke. 2012 Sep;43(9):2307-12.
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ROP in larger babies gives insight into basic mechanisms but poses a clinical challenge
Aggressive posterior retinopathy of prematurity (APROP), the most aggressive form of ROP which carries a poor prognosis despite treatment, is seen only rarely in the UK. It was formally described in 2005 1 and is thought to be confined to the most immature preterm baby when the developing retinal vessels have reached only zone I or posterior zone II. This belief was challenged most effectively by Shah et al who recently reported 2 APROP in 99 babies some of whom were 33-35 weeks gestational age (GA) and >2000 grams birthweight (BW). These babies would not have even been screened for ROP in many countries on the basis that, at this degree of maturity, retinovascular development would have reached zone III when sight-threatening ROP is no longer a risk.
So, how could sight-threatening ROP occur in these babies? The fluorescein angiograms performed on 19 of the 99 babies with APROP provide unique insight into the pathogenesis of this condition. They show that the retinal vessels which were initially observed to be in zone II and III, as would be expected of babies born at 33-35 weeks GA, later regressed to zone I so making the baby susceptible to APROP. Thus, previously formed vessels had been obliterated due to the unblended oxygen many of these babies had received. This is probably the first objective evidence in the human that hyperoxia not only halts vascular development but actually causes major retinal vessel retraction and loss. This confirms the observations of Ashton 3,4 and Patz 5,6 in the experimental animal over 60 years ago who observed that exposure to hyperoxia led to retinal arteriolar constriction, irreversible vaso-obliteration and dissolution of retinal capillary endothelial cells. This was followed by a second phase, on removal from the hyperoxia, consisting of a vasoproliferative response induced by the ischaemia due to the capillary closure of the first phase.
There are several important lessons from this case series from India. First, that the administration of unblended oxygen to babies > 32 weeks GA and >1500 g BW renders them susceptible to sight-threatening ROP, APROP in particular, an ROP type which, with a high standard of neonatal care, only affects the most immature baby and then only rarely. Second, the mean age for treatment in this study was 35.7 weeks postmenstrual age indicating that the ROP timescale is highly compressed for the larger baby as guidelines in low/middle income countries have already recommended.5 Third, and critically, these findings highlight the need to avoid the unnecessary use of supplemental oxygen, from the time of resuscitation in the delivery room onwards.
Alistair R Fielder Department of Optometry & Visual Science, City University, Northampton Square, London EC1V 0HB. firstname.lastname@example.org
Clare Wilson UCL Institute of Ophthalmology, Division of Visual Science, London EC1V 9EL
Clare Gilbert International Centre for Eye Health, London School of Hygiene and Tropical Medicine, London WC1E 7HT
References 1. International Committee for the Classification of Retinopathy of Prematurity. The International Classification of Retinopathy of Prematurity revisited. Arch Ophthalmol 2005; 123: 991-9.
2. Shah PK, Narendran V, Kalpan N. Aggressive posterior retinopathy of prematurity in large preterm babies in South India. Arch Dis Child Fetal Neonatal Ed 2012; 97 (5): F371-5.
3. Ashton N. Oxygen and retinal blood vessels. Trans Ophthalmol Soc UK 1980; 100: 359-62.
4. Patz A. Role of oxygen on immature retinal vessels. Invest Ophthalmol Vis Sci 1965; 4: 988-99.
5. Jalali S, Anand R, Kumar H, Dogra MR, Azad R, Gopal L. Programme planning and screening strategy in retinopathy of prematurity. Indian J Ophthalmol. 2003 51: 89-99.
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Measuring the wrong force leads to unjustified conclusionsDear Editor,
While commending van Vonderen et al. for an interesting and well-executed study on forces applied during mask ventilation of neonates1, I have two criticisms.
Firstly, the study was inappropriate to discover whether in compensating for mask leak, clinicians "[press] down on the mask too hard, leading to obstruction of the nose and mouth.1" In measuring the force transmitted through the manikin's head to the underlying surface they have only obtained a lower bound for the facial force. As described in their paper, the force applied to the face is due to compression between the mask and chin lift applied -- if equal, no force would be transmitted to the surface. In view of this it is not surprising they found a large variation in the baseline force, and no systematic change when participants were informed of the leak.
Secondly, there are unjustifiable assertions about the effects of this occipital force. Estimating an average pressure of 170 mmHg (for a 29-week gestation infant) between head and surface, the authors "would expect cerebral capillary blood flow to effectively cease in regions exposed to the greatest force." Not only is the fluid consistency of the neonatal brain unlikely to allow for significant pressure gradients, but the presence of the fontanelles limits increase in pressure by allowing volume displacement. Any force transmitted will be primarily through the skull. Neonates are exposed to similar pressures during normal labour, and no relationship with Apgar scores or neurobehavioural status has been found2.
Whilst the transmission of large forces through the head is unnecessary for adequate mask ventilation and unlikely to be desirable, this study provides no evidence this happens in practice, nor that it would lead to neurological damage.
To investigate the magnitude and effects of the facial and occipital forces described, this study could be repeated using transducers to measure the pressure between the mask and face during manikin ventilation, and the transmitted occipital pressure would need to be measured in real resuscitation, or preceding elective intubation.
- van Vonderen, J. J. et al. Compressive force applied to a manikin's head during mask ventilation. Arch Dis Child Fetal Neonatal Ed 97, F254-F258 (2012).
- Svenningsen, L., Lindemann, R. & Eidal, K. Measurements of Fetal Head Compression Pressure During Bearing Down and Their Relationship to the Condition of the Newborn. Acta Obstetricia et Gynecologica Scandinavica 67, 129-133 (1988).
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Do not forget cystic fibrosis
I read with interest the article by Best et al. regarding the epidemiology of small intestinal atresia. In the evaluation on the associated conditions nevertheless the Authors do not include nor mention the association of intestinal atresia with cystic fibrosis. In fact this is an association which should never be forgotten while caring for an infant with small intestinal atresia. Up to 13% of children with jejunoileal atresia (JIA) can be affected by cystic fibrosis.[1,2]. This association can indeed be frequently overlooked. Stollman et al. reviewed the medical records of 114 patients with JIA and found that 2 out of 9 patients who were diagnosed with cystic fibrosis, received the diagnosis much later in life. Furthermore the association with cystic fibrosis could partly explain the different prevalence of JIA in Europe and should be also considered in the explanation of the changes of prevalence in time. Above all I think it is important to remark that newborns with intestinal atresia should undergo genetic testing for cystic fibrosis.
1 Roberts HE, Cragan JD, Cono J, et al. Increased frequency of cystic fibrosis among infants with jejunoileal atresia. Am J Med Genet 1998;78:446-9. 2 Kumaran N, Shankar KR, Lloyd DA, et al. Trends in the management and outcome of jejuno-ileal atresia. Eur j Ped Surgery 2002;12:163-7. 3 Stollman TH, Wijnen RMH, Draaisma JMT. Investigation for cystic fibrosis in infants with jejunoileal atresia in the Netherlands: a 35-year experience with 114 cases. Eur J Pediatr 2007;166:989-90.
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"SHC" versus "WBC" in therapeutic hypothermia for HIE
Dear Editor, We read with interest the article by Sarkar et al(1) on distribution and severity of hypoxic-ischaemic lesions on brain MRI following therapeutic cooling .It is perhaps one of the very few studies which has attempted to look at the possible differences between the two forms of cooling for hypoxic ischemic encephalopathy(HIE).Brain MRI is increasingly being utilized as a good biomarker of long term neurological outcome when combined with newer advanced techniques such as diffusion weighted imaging (DWI) and proton magnetic resonance spectroscopy (MRS). We agree with the authors regarding the theoretical dangers of differential brain cooling with selective head as compared to whole body hypothermia .This seems to be the reason why many centers are now following whole body cooling(WBC) as opposed to selective head cooling(SHC) in addition to the fact that SHC is more difficult to institute. The initial trials from India too have utilized whole body cooling by indigenous use of ice-gel packs and have shown that therapeutic hypothermia is feasible and useful (2-3). With respect to the current study (1), we have the following observations which might have influenced the findings :
1. As the authors themselves have pointed out in the discussion, the neonates in the SHC group as opposed to WBC were perhaps worse at the outset itself. The data presented shows this to some extent though not statistically significant individually (i) 8/23 babies recovered from APGAR 0-3 in SHC Vs 18/36 in WBC and the details on 4 babies in SHC and 2 in WBC group with respect to APGAR is not there, either they recovered from the poor APGAR score or it was not available (ii) 23% babies in SHC group had pH < 6.7 Vs 12% in WBC (iii) clinical seizures before treatment in SHC group was 50% Vs 37% in WBC group (iv) sentinel events were 56% in SHC Vs 39% in WBC (v) abruptio placenta was 23% in SHC % Vs 12 % in WBC.
2. Other authors have also held a similar opinion regarding the patient group which entered the Cool cap trial which used aEEG as the third entry criteria and hence selected a more severe patient group which was also reflected in the a priori higher prediction of 70% poor outcome in the control group for Cool cap compared with 50% for NICHD trial. Higher incidence of seizures at enrollment in cool cap (59%) vs NICHD trial (43%)( p< 0.05 Fisher exact test ) also suggested that Cool cap population was more severely affected(4-5).
3. Again as the authors agree in the article that SHC was done in the pre-WBC era and hence must have received babies who were sicker. Acute severe asphyxia causes basal ganglia lesions and this was rare as per the authors in their analysis. Instead the injury pattern seemed like a global & prolonged asphyxia in both the groups and thus the neonates enrolled seem to have suffered a prolonged asphyxia. This could also be because both the Cool cap and NICHD babies were not cooled en-route and cooling was started at ~ 4-5 hours and target temperature achieved almost an hour later(4-5).
4. Ultimately we need randomized controlled trials using standard cooling devices/methods encompassing patient population of both the developed and developing world comparing SHC versus WBC with MRI (with DW imaging and MRS) as part of the algorithm to be able to finally address the choice of cooling method.
1.Sarkar S,Donn SM, Bapuraj JR,Bhagat I, Barks JD.Distribution and severity of hypoxic-ischaemic lesions on brain MRI following therapeutic cooling: selective head versus whole body cooling .Arch Dis Child Fetal Neonatal Ed 2012;97:F335-F339
2. Koshy B, Padankatti CS, George KC, Thomas N . Neurodevelopmental outcome following whole body cooling for perinatal asphyxia.Indian Pediatr 2011;48(12):982-3.
3. Bharadwaj SK, Vishnu Bhat B. Therapeutic Hypothermia Using Gel Packs for Term Neonates with Hypoxic Ischaemic Encephalopathy in Resource- limited Settings: a Randomized Controlled Trial. J Trop Pediatr 2012; Mar 6 published online.
4. Azzopardi D, Strohm B, Edwards AD, Halliday H, Juszczak E, Levene M, et al. Treatment of asphyxiated newborns with moderate hypothermia in routine clinical practice: how cooling is managed in the UK outside a clinical trial. Arch Dis Child Fetal Neonatal Ed 2009;94:F260-4.
5.Marianne Thoresen. Hypothermia after Perinatal Asphyxia: Selection for Treatment and Cooling Protocol .J Pediatr 2011;158:e45-9
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Re:Response to: Drugs used for comfort care after withdrawal of intensive treatment in tertiary neonatal units in the UK1.
Dear sir I am grateful for Dr. Power's comments and the opportunity to respond to them. We do know that withdrawal of intensive treatment can pose many challenges. Once decision is agreed to withdraw intensive treatment a significant time elapses before ventilatory support is withdrawn. This duration is very much dependent on individual cases and is guided by clinical, social, religious and familial factors. Respiratory support is only one aspect of intensive treatment and so do not agree with the statement that, withdrawal of intensive treatment equates to withdrawal of ventilatory support. I consider it as one of the final steps in this process. This explains the use of morphine and continuation of?neuromuscular blockers in neonates who already have been on it by some units and this is in agreement with the RCPCH guidelines. Unfortunately in our survey we didn't ask the question regarding use of drugs after ventilatory support is withdrawn. Such data would have been useful and their absence was a weakness of this survey. So our data do not reflect the use of neuromuscular blockers after withdrawal of ventilatory support by some units. Rajiv Chaudhary
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