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  2. At our unit, we routinely screen and start antibiotics if there are 2 risk factors. Prolonged rupture of membranes is 1. The others we look out for are fever in the mother more than 38C, premature onset of labour, positive GBS on HVS, features of chorioamnionitis (fetal tachycardia, maternal tachycardia, foul smelling liquor). Remember, most investigations are not helpful in the first 24 hours of the illness.
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  4. Neonatal Difficult Airway Course IAP Neocon 2020 Thrissur India The MPROvE academy UK University Hospital Southampton is organising the Difficult Neonatal Airway Course at the IAP Neocon 2020. Places are limited to 30. The course covers human resource management in management of the neonatal airway. We also cover training in Videolaryngoscopy on advanced neonatal manikins which are life like and have been developed in conjunction with LifeCast UK (https://www.lifecastbodysim.com) . The course is the first of its kind covering advanced neonatal airway techniques including use of difficult neonatal airway devices like the airtraq as well as anaesthetic techniques. The course provides accreditation in use of videolaryngoscopy as well as providing training in less invasive surfactant therapy on a specially designed preterm manikin for the same. We will provide teaching on the following in the course with hands on training modules Algorithms for management for the Difficult Neonatal Airway Management of the Difficult Neonatal Airway in the Preterm Neonate Videolaryngoscopy in Neonates Management of Pierre Robin Syndrome/ Anterior Airway Less Invasive Surfactant Management with VL Cant Intubate Cant Ventilate Algorithms Difficult Neonatal Airway Videos More details are as below Website-A course programme can be accessed here https://www.mproveacademy.com/mprove-academy/neonatal-difficult-airway-course/kerala-thrissur/02-10-2020 Course Content-A video of the the course can be obtained here https://youtu.be/Zt91I5vdlN4 Dr Alok Sharma Consultant Neonatologist Princess Anne Hospital Southampton United Kingdom MBBS MD MRCPCH CCT Paediatrics (Neonatal Medicine) UK Lead Medical Training Initiative Programme Royal College of Paediatrics and Child Health UK Member International Education Board Royal College of Paediatrics and Child Health UKDirector & Founder MPROvE Academy UK (www.mproveacademy.com) Lead Wessex-Oxford Neonatal Education Programme (www.wonepedu.com) Welcome to the Videolaryngoscopy & Difficult Neonatal Airway IAP Neocon MPROvE Academy.pptx
  5. Very good picture. Thanks.
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  7. I cannot access the full text from home, but it strikes me that intermittent hypoxia is, at best, a surrogate for the clinical indication I and my colleagues have done trials of post-pyloric feeding in this patient population. As you say, practices vary, so perhaps I'm an outlier, but I use post-pyloric feeding for the very specific subpopulation of BPD patients for whom I am trying to modulate the mode of support (eg wean the baby who is 'stuck' on a low level of CPAP or a HFNC from positive pressure to a low flow canula that can be weaned on an outpatient basis). These trials of post-pyloric feeding typically run ~1 - 2 weeks and the outcomes we follow are (in order from least to most important): intermittent hypoxemia, baseline FiO2 changes, changes in level of support. I agree that those who seldom or never resort to transpyloric feedings need not change their practice based on this study, but I'm not sure this trial addresses the way transpyloric feeding is used in my part of the world.
  8. First off I should let you know that we do not do transpyloric feeding for our infants with BPD. Having said that I am aware of some units that do. I suspect the approach is a bit polarizing. A recent survey I posted to twitter revealed the following findings: I think the data from this small poll reveal that while there is a bias towards NG feeds, there is no universal approach (as with many things in NICU). Conceptually, units that are using transpyloric feeds would do so based on a belief that bypassing the stomach would lead to less reflux and risk of aspiration. The question though is whether this really works or not. New N of 1 Trial I don’t think I have talked about N of 1 trials before on this site. The trials in essence allow one patient to serve as a study unto themselves by randomizing treatments over time for the single patient. By exposing the patient to alternating treatments such as nasogastric or nasoduodenal feedings one can look at an outcome and get a sense of causality if a negative or positive outcome occurs during one of the periods consistently. That is what was done in the study Individualising care in severe bronchopulmonary dysplasia: a series of N-of-1 trials comparing transpyloric and gastric feeding by Jensen E et al from the Children’s Hospital of Philadelphia. The authors in this study determined that using a primary outcome of frequency of daily intermittent hypoxaemic events (SpO2 ≤80% lasting 10–180 s) they would need 15 patients undergoing N of 1 trials between nasogastric and nasoduodenal feeding. Included infants were born at <32 weeks and were getting positive airway pressure and full enteral nutrition at 36 0/7 to 55 6/7 weeks PMA. Infants who were felt to be demonstrating signs of reflux or frank regurgitation were enrolled. The findings Thirteen of 15 enrolled patients completed the study. The two who did not complete did so as their oxygen requirements increased shortly after starting the trial and the clinical team removed them and chose their preferred route of feeding. Randomization looked like this: Of the 13 though that completed and using an intention to treat analysis of the other two the findings were somewhat surprising. Contrary to what one might have thought that transpyloric would be a lung protective strategy, the findings were opposite. Overall the combined results from these 15 patients demonstrated that nasogastric feedings were protective from having intermittent hypoxic events. How can this be explained? To be honest I don’t really know but it is always fun to speculate. I can’t help but wonder if the lack of milk in the stomach led to an inability to neutralize the stomach pH. Perhaps distension has nothing to do with reflux and those with BPD who have respiratory distress with some degree of hyperinflation simply are prone to refluxing acid contents due to a change in the relationship of the diaphragmatic cura? It could simply be that while the volume in the stomach is less, what is being refluxed is of a higher acidity and leads to more bronchospasm and hypoxemic events. What seems to be clear even with this small study is that there really is no evidence from this prospective trial that transpyloric feeding is better than nasogastric. Given the size of the study it is always worth having some degree of caution before embracing wholeheartedly these findings. No doubt someone will argue that a larger study is needed to confirm these findings. In the meantime for those who are routinely using the transpyloric route I believe what this study does at the very least is give reason to pause and consider what evidence you have to really support the practice of using that route.
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  10. Dear colleagues! Hope you all are doing well in 2020 :). Maybe anyone has an experience of using nebulisers in SLE 6000 and Leoni Plus ventilators? Some of our old machines need to be replaced and we have to make our choice about new ones. In good old and simple Newport E100 (reliable as Kalashnikov rifle by the way) there is a special port for nebuliser, making additional flow in circuit when activated. You only need a tube with medication's camera attaching to the Y-piece of the circuit and to switch on the particular button. How is it working for SLE 6000 and new Leoni Plus ventilators? The same way, or not? As far as I understood SLE has separate nebulisation port but I failed to find any button for nebulisation in manual. About Leoni I know even less :(. Do you always need to buy additional stuff like Aeroneb for SLE6000 or LM M-neb for Leoni? Unfortunately I cannot understand this by myself from Internet resources. Many thanks!
  11. I refer adrenalida aerosolized. 1 / 1000. Just after extubation. In very preterm newborn.
  12. Inhaled nitric oxide has been around for some time now. I recall it being called at one point in medical school “endothelial relaxation factor” and then later on identified as nitric oxide. Many years later it finds itself in common usage in NICUs all over the world. Our experience though has been for treatment of pulmonary hypertension and for that it is pretty clear that for those afflicted by that condition it can be lifesaving. Over the years other uses have been looked at including prevention of BPD (turned out not to be the case). Rescue approaches therefore have found to be useful but on the prophylactic side of things not so much. Maybe starting earlier is the key? A group based out of Oklahoma has published a pilot study that raised an eyebrow for me at least. Krishnamurthy et al released Inhaled Nitric Oxide as an Adjunct to Neonatal Resuscitation in Premature Infants: A pilot, double blind, randomized controlled trial . The study set out to recruit 40 infants who between 30-90 seconds of life if requiring PPV would either get iNO 20 ppm with 30% oxygen or 30% oxygen and placebo for ten minutes. At ten minutes weaning of iNO by 1 ppm per minute for a total of 17 minutes was done. The primary outcome of interest was FiO2 required to achieve target oxygen saturations. As with many studies that seek enrollment prior to delivery this study was a challenge as well with early termination of the study after 28 babies (14 in each group) were recruited. Did they find anything interesting? In spite of the low numbers in the study, the authors did find a divergence in the FiO2 needed to achieve the target oxygen saturations. The authors conclusions were that the cumulative exposure to FiO2 was lower in the iNO group as well as the maximum exposed FiO2 of 39% vs 48% (although this almost but not quite met statistical significance. Even then this is a pilot study so inferring too much could be a dangerous thing. The study though does get one thinking but we need to be wary of letting our brains do some mental trickery. Lower FiO2 seems like a good thing given what we know about oxygen free radicals. What about rapid lowering of pulmonary vascular resistance with exogenous iNO? Is this a good thing or could other things be lurking around the corner? Could a larger study for example find a higher rate of pulmonary hemorrhage with rapid reductions in PVR? The authors did not find harm in the study but again with small numbers it is hard to conclude too much. What this small study does though is raise many questions that I think could be interesting to answer. If a patient needs less FiO2 at 17 minutes after study entry might there be less perceived need for higher PEEP if ventilated or CPAP levels if on non-invasive support? Less pressure could lead to less risk of pneumothorax (or more perhaps if under treated but with respiratory distress. Less pressure might also influence longer term risks of BPD from barotrauma or volutrauma for that matter. Regardless this is only the beginning. I have no doubt there will be further trials on the way. The trick will be as in this study to obtain consent unless a deferred consent could be obtained but I have my doubts about getting that. Nonetheless, wait for more to come!
  13. Only when showing post-extubation stridor agree with @bimalc Although, @Pototo I would like to know did you mean Racemic epinephrine (before or after extubation)?
  14. Good evening doctors .. We practice that premature rupture of membranes more than 16 hour we should investgate baby for possible sepsis even if he is clinically good in 1 st 24 hours because infection may start to manifest after 2 or 3 days ...but what if the history of mother is only leakge for couple of days can this be considered PROM ? 🤔 Thanks in advance 🙂
  15. Every international society i check i found the 1st recommended link is 99nicu.org 👍
  16. A colleague of mine has one such probe and said she would let me try it ( after New years). Will report back!
  17. I have contacted the company before. They said it's not designed or licensed for newborns and I have not come across anyone that have used it before.
  18. I think it's fairly reasonable to attribute the baby's seizures at 12 hours to an etiology other than HIE. The cord gas is ok and also the gas at 1 hour can be attributed to the resuscitation YES. But it could be also respiratory as you have not mentioned the PCo2. And again regarding the gas at 1 hour of life... It's not that acidotic to start cooling ( Looking at the CPS statement of 7.15) I think guidelines are made for those situations ...to help when things get blurry. Sticking to it as is the right thing for me until an alternative approach has established evidence behind it.
  19. I agree with Martin And regarding the values for a ventilated baby... Usually a minimum of 7.25 with a pco2 of 45-55 and not to exceed 75 as it is associated with a poor neurodevelopmental outcome. These values are independent of gestational age and weight.
  20. Dear collagues In our nursery we use BabyFlow from Dräger to provide NIV via VN500. We are planning to introduce the Seattle-PAP system (a bubble CPAP system) from Dräger to deliver nCPAP. Previously we have used beneveniste-CPAP. So moving to BabyFlow is quite a big step as the headgear and interface is quite different and much more bulky compared to what we have used for many years. Is there anyone out there using BabyFlow who would be willing to share experience? Our nurses are working hard to get used to the nasal interface and fixation system and especially when using bubbleCPAP we have lots of difficulties with leakage. many thanks in advance cheers Christian A few words about the unit: Level 3 NICU in Denmark. From 23 weeks GA to term+, noninvasive resp support and Conventional and HFO ventilation, iNO, ECMO, cardiac and pediatric surgery on site in addition to ENT, ortho and neurosurgical surgery and retrieval service
  21. thank you very much for your reply and in the narrow range of weight and gestational age, which values of ph make reference as the minimum objective
  22. I have observed this repeatedly in babies whose mothers were taking SSRI antidepressants, specifically Zoloft. Happy baby who does not cry. Cheers, MK
  23. Great question, Juan Carlos. I am partial to the VN500, but I'm sure both devices can deliver VG quite well. The problem is that babies don't like to be acidotic. Consequently, there is a problem with permissive hypercapnea in the first days of life in small preemies, because their kidneys are not able to compensate for respiratory acidosis. Therefore, the baby will try to generate a tidal volume sufficient to bring the PCO2 down and normalize the pH. As you know when the tidal volume exceeds the target value, PIP will come down and pretty soon, your baby may be on endotracheal CPAP with rising oxygen requirement (due to the drop in MAP), tachypnea and increased work of breathing. You would have to sedate the baby sufficiently to suppress their respiratory drive, which is a bad idea. People find all kinds of ways to reduce the support for the baby's effort, for example changing from AC to SIMV at a low rate, so the baby is unable to generate adequate minute ventilation and correct the acidosis. So, the baby is struggling, but the doctor is happy, because the PCO2 is where he or she wants it. If you can buffer the acidosis by adding some acetate to your TPN and get the pH up to near normal, you might be able to let the CO2 rise gradually. The focus needs to be on pH, not PCO2, because it's the pH that is the primary stimulus for respiratory drive. Basically it is better to support the baby's effort to maintain normal pH and avoid the mistake of looking only at the PCO2. Ultimately, it is the perivascular pH that controls cerebral circulation, but unfortunately all studies keep focusing on PCO2 and ignoring pH. What we know is that rapid fluctuations in PCO2 confer the greatest risk of IVH. Once the baby is a bit older and the kidneys are more mature, it'a s lot easier to allow permissive hypercapnia if they still need mechanical ventilation. I hope this helps, MK
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    • At our unit, we routinely screen and start antibiotics if there are 2 risk factors. Prolonged rupture of membranes is 1. The others we look out for are fever in the mother more than 38C, premature onset of labour, positive GBS on HVS, features of chorioamnionitis (fetal tachycardia, maternal tachycardia, foul smelling liquor). Remember, most investigations are not helpful in the first 24 hours of the illness. 
    • Neonatal Difficult Airway Course IAP Neocon 2020 Thrissur India The MPROvE academy UK University Hospital Southampton is organising the Difficult Neonatal Airway Course at the IAP Neocon 2020. Places are limited to 30. The course covers human resource management in management of the neonatal airway. We also cover training in Videolaryngoscopy on advanced neonatal manikins which are life like and have been developed in conjunction with LifeCast UK (https://www.lifecastbodysim.com) . The course is the first of its kind covering advanced neonatal airway techniques including use of difficult neonatal airway devices like the airtraq as well as anaesthetic techniques. The course provides accreditation in use of videolaryngoscopy as well as providing training in less invasive surfactant therapy on a specially designed preterm manikin for the same. We will provide teaching on the following in the course with hands on training modules Algorithms for management for the Difficult Neonatal Airway Management of the Difficult Neonatal Airway in the Preterm Neonate Videolaryngoscopy in Neonates Management of Pierre Robin Syndrome/ Anterior Airway Less Invasive Surfactant Management with VL Cant Intubate Cant Ventilate Algorithms Difficult Neonatal Airway Videos More details are as below Website-A course programme can be accessed here https://www.mproveacademy.com/mprove-academy/neonatal-difficult-airway-course/kerala-thrissur/02-10-2020 Course Content-A video of the the course can be obtained here https://youtu.be/Zt91I5vdlN4   Dr Alok Sharma Consultant Neonatologist Princess Anne Hospital Southampton United Kingdom MBBS MD MRCPCH CCT Paediatrics (Neonatal Medicine) UK Lead Medical Training Initiative Programme Royal College of Paediatrics and Child Health UK Member International Education Board Royal College of Paediatrics and Child Health UKDirector & Founder MPROvE Academy UK (www.mproveacademy.com) Lead Wessex-Oxford Neonatal Education Programme (www.wonepedu.com) Welcome to the Videolaryngoscopy & Difficult Neonatal Airway IAP Neocon MPROvE Academy.pptx
    • Very good picture. Thanks.
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