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  3. I think my first training in resuscitation began with the principles outlined in the NRP 3rd edition program. As we have moved through subsequent editions with the current edition being number 7, I can’t help but think about how many changes have occurred over that time. One such change has been the approach to using medications as part of a resuscitation. Gone are such things as calcium gluconate, naloxone and sodium bicarbonate but something that has stood the test of time is epinephrine. The dosing and recommendations for administering epinephrine have changed over time as well with the dose of endotracheal medication increasing from 0.01 to 0.03 and now to 0.05 – 0.1 mg/kg. While this dosing has increased, that of IV administration has remained the same at 0.01 to 0.03 mg/kg. The change in dosing for the ETT route was due to an increasing awareness that this route just isn’t as effective as IV. Having said that with only 0.1% of resuscitations requiring such support the experience with either route is fairly limited. What is the concern? Giving a medication directly via the IV route ensures the dose reaches the heart in the amount desired. In the case of ETT administration there are a few potential issues along the way. The first is that one needs to push the dose down the ETT and this presumes the ETT is actually in the trachea (could have become dislodged). Secondly, if the medication is sent to the lung what effect does the liquid component in the airways have in terms of dilution and distribution of the medication? Lastly, even if you get the epinephrine to the lung it must be picked up at the capillary level and then returned to the left side of the heart. In the absence of significant forward pulmonary blood flow this is not assured. What is the evidence? In terms of human clinical research it remains fairly limited. Barber published a retrospective review of 47 newborns who received epinephrine via the endotracheal route. The study Use and efficacy of endotracheal versus intravenous epinephrine during neonatal cardiopulmonary resuscitation in the delivery room found that spontaneous circulation was restored in 32% of this cohort. Following the first dose, a subsequent dose of intravenous epinephrine restored circulation in 77%. This study provided the first suggestion that the IV route may be better than endotracheal. Keep in mind though that this study was retrospective and as the authors conclude in the end, prospective studies are needed to confirm these findings. The question really is what is the likelihood of restoring circulation if the first dose is given IV? Eleven years later we have a second study that attempts to answer this question although once again it is retrospective. Efficacy of Intravenous and Endotracheal Epinephrine during NeonatalCardiopulmonary Resuscitation in the Delivery Room by Halling et al. This study really was designed to answer two questions. The study group looked at the period from July 2006 to July 2014. During this period the dose of IV epinephrine remained unchanged as per NRP recommendations but the dose of endotracheal epinephrine increased from 0.01 to 0.03 and then to 0.05 mg/kg endotracheally. The increase was in response to both NRP and site observations that the lower doses were not achieving the effect they were hoping for. The Results ETT epinephrine IV Epinephrine Number 30 20 Return of circulation 23 15 1 dose 6 4 2 dose 5 8 3 doses 9 0 4 doses 3 3 In the ETT group all doses except for 3 after the first dose were given as IV. There was no difference in the response rate over time suggesting that higher doses do not truly increase the chance of a better response. The authors noted that the effectiveness of the two arms were not that different despite a significantly higher dose of epinephrine being administered to the group receiving ETT epinephrine first which is not surprising given the higher recommended dosages. What I find interesting though is that giving the first dose of epinephrine was given IV in 20 of the paitents, if it is indeed the better route one might expect a better response than in the ETT group. The response from one dose of ETT epi was 20% while that from the IV first group was in fact also only 20%! We do indeed need to be careful here with small numbers but the results at least to me do not suggest strongly that giving IV epi first ensures success. What the study suggests to me is that two doses of epinephrine may be needed to restore circulation. If you choose to start with IV it certainly does not seem unwise but if you have any delays I don’t see any reason to avoid ETT epinephrine as your first line. The reality is that for many individuals a UVC is a procedure that while they may have learned in an NRP class they may have never actually placed one. Having an ETT in place though seems like a good place to start. I doubt we will ever see a randomized trial of ETT vs IV epinephrine in Neonatology at this point given the stance by the NRP so these sorts of studies I suspect will be the best we get. For now, based on what is out there I suggest use the route that you can get first but expect to need additional doses at least one more time to achieve success. Lastly remember that even if you do everything correct there will be some that cannot be brought back. Rest assured though that if the first dose was given via ETT you have still done your best if that was the route you had.
  4. Good job. Thanks Stefan Sent from my iPad using Tapatalk
  5. Thanks a lot for this interesting knowledge. I will propose an update to our protocol for hypothermia-HIE.
  6. no.Baby didn't have UVC
  7. Click on this link for author updates- http://createsend.com/t/d-48647D6A56FF9751
  8. The 17th Annual Saudi Neonatology Society Conference was held 11-13 April, 2017. All lectures, including the four lectures I had, were recorded and is now available as a Youtube channel. Please find the link below! http://www.youtube.com/playlist?list=PLJ8UU7ncYL9R7J8LWUXswkil8TVur9EDS
  9. Earlier
  10. @selvanr4 As I have understood, the etiology is commonly unknown (although UVC is a risk factor) and the outcome is generally also good. Given that liver function is maintained reasonably well, the liver and venous flow will recover over time (recann or new routes) To my knowledge, anticoagulation is not know to work. I have this article in my collection, I guess there are newer reviews out there though: https://www.ncbi.nlm.nih.gov/pubmed/21925985
  11. Did the baby have a UVC
  12. We recently had a newborn referred with hepatic vein thrombosis. Baby had blood and mucoid stools. The total count was high and hence blood c&s sent and commenced with i v antibiotics.symptoms abated. no organism grown in culture. We were hesitant to start LMW heparin because of diverse opinions.But continued with iv antibiotics. Rpt ultrsound showed developing collaterals. What is the probability that the child will /will not have chronic liver disease. Can LMW Heparin melt away the thrombosis? thanks selvan rathinasamy
  13. Many of you may already have come across the "Practical Ultrasound for the Neonatologist" software. Professor Nick Evans at the Royal Prince Alfred Hospital in Sydney, Australia, just reminded us the good news that these education programs, one on echocardiography and one on brain ultrasound, is no longer distributed on CD-roms, but is available as digital downloads. Prices are only 25 AUD (about 17 euro) each. The programs are currently only available for Windows. The direct link to the on-line shop is https://practical-neonatal-ultrasound.selz.com/ All profits go to support teaching and research in neonatal haemodynamics. The link to the department is http://www.slhd.nsw.gov.au/rpa/neonatal/default.html
  14. Please add me to the whatsap group
  15. The backside of whatsup is the limitation of users within a group. We believe that quite many people may join the 99nicu Slack channels
  16. Very good shift although whatsapp is also very good alternative
  17. The PREMILOC trial was a multi-center RCT of hydrocortisone, 0.5mg/kg twice per day for 7 days followed by 0.5 mg/kg per day for 3 days, given starting within 24 hours of age to infants of 24 to less than 28 weeks gestation. Neurological and developmental follow-up has just been published (Baud O, et al. Association between early low-dose hydrocortisone therapy in extremely preterm neonates and neurodevelopmental outcomes at 2 years of age. JAMA. 2017;317(13):1329-37.) There were 523 infants initially enrolled and 406 who survived to 2 years of age, 93% of those were seen at between 21 and 23 months corrected age, for examination and evaluation with standardized instruments. You probably remember that the primary outcome of the trial was survival without BPD, which was somewhat reduced by the intervention (51% compared to 60% in controls). This was as a result of fewer deaths (18% compared to 23%) and less BPD (22% compared to 26%) neither of which component of the primary outcome was individually significant. In this follow-up study the authors not that after the 36 week end of the main data collection there were a further 8 deaths, 7 in the control group and 1 in the hydrocortisone group, 5 of which were from severe BPD (4 vs 1). (These deaths were also reported as the deaths before discharge in the initial publication, but I don't think the causes were noted). All of the babies followed had a standardized neurologic evaluation, but unfortunately only 80% of them had the revised Brunet-Lézine evaluation of developmental progress, which gives a developmental quotient, standardized, as usual, with a population mean of 100 and SD of 15. Basically there were no differences between the groups on neurological signs of impairment, or developmental scores. For example there were 6% of the hydrocortisone and 5% of the control group who developed cerebral palsy. Mean Global Development score was 91.7 in the hydrocortisone group and 91.4 in the control group. I guess one could say that if there is less BPD and no increase in neuro or developmental adverse effects, we should think of using this as routine therapy? But the group also report clinically important respiratory outcomes up to 2 years of age : You can see from their table 2 that there is no sign of better respiratory health (or incidentally any effect on growth outcomes) among the survivors, with some of the minor differences being in one direction, some in the other direction. Which calls into question again the use of oxygen at 36 weeks, as an outcome for RCTs even when combined with an oxygen reduction test, as in this trial. If kids are more likely to be out of oxygen at 36 weeks, but no more likely to go home on oxygen (14 babies in each group) and not more likely to have respiratory problems in follow-up, then the significance of getting extubated earlier, or needing oxygen for fewer days is questionable, at least the significance to families. I think those outcomes are indeed benefits to families, its much better to see your baby with CPAP or non-invasive ventilation than intubated, but if there is on clear long-term benefit then we should be pretty certain that there is no harm before instituting this as routine therapy. Currently, is there any other evidence of harm from this approach? In the initial data from this trial, late onset sepsis was higher (31% vs 25% had at least one episode), NEC was higher (7% vs 5%) GI perforation was higher (5% vs 4%) use of insulin for hyperglycemia was higher (38% vs 34%) and severe RoP was higher (2% vs 1%) all of which could be due to chance effects, but the study was not powered to detect such small, but potentially important, differences; indeed in one subgroup, the most immature infants, the impact of steroids on late onset sepsis was, indeed quite different, 40% vs 23%, and their analysis showed this was unlikely due to chance. Its interesting in the on-line supplementary appendix that the major difference in late onset sepsis arose after the end of the treatment period. It is also interesting that this dose of hydrocortisone had no evident impact on blood pressures, nor on the use of dopamine. I think that all of these worrying differences between the groups, favoring control, with no evidence of long-term benefit, and the only evidence of short-term benefit being shorter intubation and shorter duration of oxygen therapy, that we should not introduce this regime as a routine in our patients. There is a minor difference in survival with the hydrocortisone treatment though, with 19% mortality before discharge (and before 2 years) compared to 25% in the control group. I calculate the 95% confidence intervals of this 6% difference as being between 13% fewer deaths and 1% more deaths, using early low dose hydrocortisone in similar babies. Unfortunately, I think I have to say that this therefore warrants further study. A larger trial with enough power to detect a 5% difference in mortality, perhaps in a region where the survival at 24 and 25 weeks is above 65% (as in this French multi-center trial; compared to for example 78% in the CNN database from 2015) should be performed. I think a future trial should not use this as a definition of bronchopulmonary dysplasia, other definitions have been suggested, such as this recent publication from the CNN (Isayama T, et al. Revisiting the Definition of Bronchopulmonary Dysplasia: Effect of Changing Panoply of Respiratory Support for Preterm Neonates. JAMA Pediatr. 2017;171(3):271-9.) In this study the best discrimination between those who had serious respiratory morbidity after discharge (when seen at 18 month follow up) from data collected during the neonatal period, was the need for oxygen or respiratory support (anything that gave positive pressure including high-flow cannulae at more than 1.5 litres per minute) at 40 weeks post-menstrual age. Serious respiratory morbidity was defined as either (1) 3 or more rehospitalizations after NICU discharge owing to respiratory problems (infectious or noninfectious); (2) having a tracheostomy; (3) using respiratory monitoring or support devices at home such as an apnea monitor or pulse oximeter; and (4) being on home oxygen or continuous positive airway pressure at the time of assessment between 18 and 21 months corrected age. Just as important, a recognition that lung injury in the newborn is a continuous spectrum, and that artificially dividing that into 2 categories, with and without lung injury is an artificial distinction designed to aid research design, not to help babies, or their families. A description of long term respiratory morbidity between groups is essential, rather than a label based on an intermediate outcoem. Mortality, in contrast, is truly a dichotomous outcome, and if it can possibly be improved by low dose early hydrocortisone, than we should pursue that possibility with more studies.
  18. The deadline to sign up for the conference is approaching! I hope to see many of you follow 99nicu'ers in Stockholm!
  19. We now 99nicu to Slack Find more info on the link below. To be added there, send me or @Francesco Cardona a message or email info@99nicu.org You can also respond to this thread, please include the email address we shall send the invite to. The team address is 99nicu.slack.com
  20. Although 99nicu.org has a great mobile interface, we lack a dedicated smartphone app. I had a very good discussion with a few colleagues recently that were using Whatsup for chat communication with other neonatologists, and they suggested 99nicu should also start an alternative channel for more simple smartphone communication. As we want to make room for quite a number of people, we have choosen Slack.com as the technical platform for this extension of the 99nicu community. While keeping the simplicity of chatlike smartphone use, it is still possible to organise discussions into "channels" and "threads" What shall we use Slack for? It is all up to us but as there is push notifications directly to the smartphone, I believe we use Slack for patient discussions, when we need prompt advice. To join the 99nicu Slack Channel, you first need to download the Slack app to your mobile. Then we just need to invite you one by one So, if you want to join, message me or @Francesco Cardona , or simply email info@99nicu.org The team address is 99nicu.slack.com
  21. The human body truly is a wondrous thing. Molecules made from one organ, tissue or cell can have far reaching effects as the products take their journey throughout the body. As a medical student I remember well the many lectures on the kidney. How one organ could control elimination of waste, regulate salt and water metabolism, blood pressure and RBC counts was truly thought provoking. At the turn of the century (last one and not 1999 – 2000) Medical school was about a year in length and as the pool of knowledge grew was expanded into the three or four year program that now exists. Where will we be in another 100 years as new findings add to the ever growing volume of data that we need to process? A good example of the hidden duties of a molecule is erythropoetin (Epo) the same one responsible from stimulating red blood cell production. Double Duty Molecule In saying that I am simplifying it as there are likely many processes this one hormone influences in the body but I would like to focus on its potential role in neuroprotection. In 1999 Bernaudin Et al performed an animal study in mice to test this hypothesis. In this elegant study, strokes were induced in mice and the amount of Epo and Epo receptors measured in injured tissues. Levels of both increased in the following way “endothelial cells (1 day), microglia/macrophage-like cells (3 days), and reactive astrocytes (7 days after occlusion)”. To test the hypothesis that the tissues were trying to protect themselves the authors then administered recombinant human Epo (rhEpo) to mice prior to inducing stroke and the injury was clearly reduced. This established Epo as a potential neuroprotectant. Other animal studies then followed demonstrating similar findings. A Human Trial When you think about hypoxic ischemic encephalopathy (HIE) you can’t help but think of whole body cooling. The evidence is pretty clear at this point that cooling in this setting reduces the combined outcome of death or neurodevelopmental disability at 18 months with a number needed to treat of 7. The risk reduction is about 25% compared to not those not cooled so in other words there is room to improve. Roughly 30-40% of infants who are cooled with moderate to severe HIE will still have this outome which leaves room for improvement. This was the motivation behind a trial called High-Dose Erythropoietin and Hypothermia for Hypoxic-Ischemic Encephalopathy: A Phase II Trial. This was a small trial comparing 50 patients (24 treated with rhEpo and cooling to 26 given placebo) who were treated with 1000 U of rEpo on days 1,2,3,5 and 7. Primary outcome was neurodevelopment at 12 months assessed by the Alberta Infant Motor Scale (AIMS)and Warner Initial Developmental Evaluation. A significant improvement in a subset of mobility on the latter was found and a significant difference in the AIMS overall. An additional finding giving support for a difference was that blinded reviews of MRI scans demonstrated a singificant improvement in brain tissue in those who received rhEPO. One curious finding in this study was that the mean timing of administration of rhEPO was 16.5 hours of life. Knowing that the benefit of cooling is best when done before 6 hours of age one can only wonder what impact earlier administration of a neuroprotective agent might have. This suggests that the addition of rEPO to cooling has additional impact but of course being a small study further research is needed to corroborate these findings. The Next Step This past week Malla et al published an interesting paper to add to the pool of knowledge in this area; Erythropoietin monotherapy in perinatal asphyxia with moderate to severe encephalopathy: a randomized placebo-controlled trial. This study was done from the perspective of asking if rhEPO by itself in resource poor settings without access to cooling in and of itself could make a difference in outcome for patients with HIE. This was a larger study with 100 Hundred term neonates (37 weeks or greater) with moderate or severe HIE. Fifty were randomized by random permuted block algorithm to receive either rhEPO 500 U kg− 1 per dose IV on alternate days for a total of five doses with the first dose given by 6 h of age (treatment group) or 2 ml of normal saline (50 neonates) similarly for a total of five doses (placebo group) in a double-blind study. The primary outcome was combined end point of death or moderate or severe disability at mean age of 19 months and the results of this and other important outcomes are shown below. Outcome Treatment Placebo p Death/disability (mod/severe HIE) 40% 70% 0.003 Death/disability (mod HIE only) 21% 61% 0.004 Cerebral Palsy 23% 45% 0.04 MRI abnormalities 40% 60% 0.04 Seizures treatment at 19 months 19% 43% 0.03 To say that these results are impressive is an understatement. The results are on par with those of cooling’s effect on reduction of injury and improvement in outcome. When looking at the primary outcome alone the result in dramatic when put in perspective of looking at number needed to treat which is 4! This is significant and I can’t help but wonder if the impact of this medication is at least in part related to starting the dosing within the same window of effectiveness of therapeutic hypothermia. Importantly there were no adverse effects noted in the study and given that rhEpo has been used to treat anemia of prematurity in many studies and not found to be associated with any significant side effects I would say this is a fairly safe therapy to use in this setting. Next Steps I find this puts us in a challenging position. The academic purists out there will call for larger and well designed studies to test the combination of rhEPO and cooling both initiated within 6 hours of age. While it takes years to get these results might we be missing an opportunity to enhance our outcomes with this combination that is right in front of us. The medication in question other than raising your RBC count has little if any side effects especially when given for such a short duration and by itself and possibly with cooling increases the rate of neuroprotection already. I don’t know about you but I at least will be bringing this forward as a question for my team. The fundamental question is “can we afford to wait?”
  22. This post rings in another new video to add to the series on the All Things Neonatal YouTube channel. I hope that you have gotten something out of the ones posted so far and that this adds something further to your approach to neonatal care. The Golden Hour Revisited In the last post to the video selections the main thrust of the video was on the use of the Golden Hour approach to starting a baby on CPAP. Having a standardized checklist based approach to providing care to high risk newborns improves team functioning for sure. What do you do though when you need to hand off a patient to another team? Depending on where you work this may not be an issue if the team performing the resuscitation is the team providing the care for the patient in the NICU. Perhaps you work in a centre similar to our own where the team performing resuscitation is not the same as the one who will ultimately admit the patient. You may also be in a location where there are no babies born on site but rather all patients are transferred in so in each case the patient is new to everyone on the receiving team. How do you ensure that a complete hand over is done. Out with the old and in with the new! By no means do I want to imply that it is not possible to transfer information outside of the way that we demonstrate in this video. What I do believe though is that with telehealth being available in more and more settings or without a formal support for the same, the use of smartphones make video conferencing a reality for almost everyone. In most centres handovers have followed the practice of like communicating with like. Nurses give report to nurses, respiratory therapists to each other and MDs to MDs. What if there was another way though? In the video below we demonstrate another approach. Would it work for your team? As you can tell I am a big fan of simulation in helping to create high functioning teams! More of these videos can be accessed on my Youtube channel at All Things Neonatal YouTube To receive regular updates as new videos are added feel free to subscribe! Lastly a big thank you to NS, RH and GS without whom none of this would have been possible!
  23. As I wrote in a previous blog post, I am involved in a very exciting, sort of a medical underground project, about providing GMP-produced probiotics for preterm infants. The non-profit company Neobiomics will provide a probiotics product in early 2018, fulfilling specific needs for preterm infants. Non-profit refers to that any potential revenue is re-invested in next generation products or leads to a price reduction. The idea is to have a self-propelling business, without commercial interests. Due to rigorous quality standards (GMP + "Infant grade") and small production batch size we estimate a price of 3 euros per stickpack, i.e. the monthly cost will be around 90 euros/infant. Given larger batches (more people use the product), we expect the price to drop in the future. To make the final internal decision on setting up the production line and produce the first batch, we need to gather information on potential use of this product. If you are interested to use the Neobiomics Probiotics product, “from the community – to the community”, please respond to a few upcoming questions that you find on this URL: https://www.surveymonkey.com/r/neobiomics It takes about 1-2 minutes to respond.
  24. My interpretation of the GRADE review is to ignore the pooled estimates for the observational studies for sure because of the poor quality. The issue is, as Stefan highlights, confounding by indication. The available RCT data do not support transfusion as increasing risk of NEC. I think the most elegant study to try and better understand what is going on and by-pass the confounding by indication study is the JAMA https://www.ncbi.nlm.nih.gov/pubmed/?term=26934258 where they are able to parse out anemia from transfusion. I am still only a fellow, but I base my transfusion practice vis a vis NEC risk on the RCT data from the GRADE review and this paper highlighting the anemia as the key feature. This conclusion is consistent with the finding in the RCTs of less NEC in the liberal transfusion group because the liberal transfusion group would presumably have less (and likely less severe) anemia.
  25. thanks for the the link
  26. I agree, if you also read the blog post by @AllThingsNeonatal above, I believe that the topic still interesting. After all, NEC is such a multifactorial disease.
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