99nicu... Your Forum in Neonatology!

Welcome to 99nicu, the web community for staff in neonatal medicine!

Become a member for full access to all features: get and give advice in the forums, start your own blog and enjoy benefits! Registration is free :) - click here to register!

Greetings from the 99nicu HQs

All Activity

This stream auto-updates   

  1. Yesterday
  2. Ours is a small unit.i have used paracetamol for ductal closure in babies with low platelets. In one neonate with stage 1 a nnec. Used rectal route. We Were able to tide over the crisis .ductal closure achieved and features of ccf subsided.
  3. Both studies are really stimulating.thanks
  4. Last week
  5. Thanks for a great post! I agree very much about the discussions in the NICU about BPD, in our unit not so much about the definition but how to manage it. As we tend to increase the saturation targets, and BPD is defined by oxygen supplementation at a certain time point, we likely increase the incidence of BPD only by setting a higher saturation target. Naturally, babies with bad lungs are at risk of doing less well in developmental terms. But the lungs or the BPD-definition may not the problem itself, more a proxy for a high-risk scenario. Related to this blog post, I started a discussion in the lung forum about saturation targeting, find it below
  6. There is some relatively strong data supporting a saturation target at 90-95%, at least during intensive care (level-3 settings) and for extremely preterm infants. This commentary from EBNEO is quite interesting: https://ebneo.org/2017/02/oxygen-saturation-targets-in-extremely-preterm-infants/ However, the studies on saturation targeting has some methodological aspects that is also good to consider. Have a look on a lecture by Barbara Schmidt below, a lecture that problematize the evidence. Further, what shall we target in the majority of preterm infants not born extremely preterm, and cared for in level-2 settings? Like a 31- or a 34-week infant who may need CPAP and supplemental oxygen only for a few days. Another common discussion is what alarm limits should be applied. If the target is 91-95&, does the alarm need to go off at 89 and 97%? Please complete the poll above on saturations targets and alarm limit, and comment below.
  7. Manufacturer of NICU equipment, like intravessel catheters.
  8. As a Neonatologist I doubt there are many topics discussed over coffee more than BPD. It is our metric by which we tend to judge our performance as a team and centre possibly more than any other. This shouldn't be that surprising. The dawn of Neonatology was exemplified by the development of ventilators capable of allowing those with RDS to have a chance at survival. As John F Kennedy discovered when his son Patrick was born at 34 weeks, without such technology available there just wasn't much that one could do. As premature survival became more and more common and the gestational age at which this was possible younger and younger survivors began to emerge. These survivors had a condition with Northway described in 1967 as classical BPD. This fibrocystic disease which would cripple infants gave way with modern ventilation to the "new bpd". The New BPD The disease has changed to one where many factors such as oxygen and chorioamnionitis combine to cause arrest of alveolar development along with abnormal branching and thickening of the pulmonary vasculature to create insufficient air/blood interfaces +/- pulmonary hypertension. This new form is prevalent in units across the world and generally appears as hazy lungs minus the cystic change for the most part seen previously. Defining when to diagnose BPD has been a challenge. Is it oxygen at 28 days, 36 weeks PMA, x-ray compatible change or something else? The 2000 NIH workshop on this topic created a new approach to defining BPD which underwent validation towards predicting downstream pulmonary morbidity in follow-up in 2005. That was over a decade ago and the question is whether this remains relevant today. Benchmarking I don't wish to make light of the need to track our rates of BPD but at times I have found myself asking "is this really important?" There are a number of reasons for saying this. A baby who comes off oxygen at 36 weeks and 1 day is classified as having BPD while the baby who comes off at 35 6/7 does not. Are they really that different? Is it BPD that is keeping our smallest babies in hospital these days? For the most part no. Even after they come off oxygen and other supports it is often the need to establish feeding or adequate weight prior to discharge that delays things these days. Given that many of our smallest infants also have apnea long past 36 weeks PMA we have all seen babies who are free of oxygen at 38 weeks who continue to have events that keep them in hospital. In short while we need to be careful to minimize lung injury and the consequences that may follow the same, does it matter if a baby comes off O2 at 36, 37 or 38 weeks if they aren't being discharged due to apnea or feeding issues? It does matter for benchmarking purposes as one unit will use this marker to compare themselves against another in terms of performance. Is there something more though that we can hope to obtain? When does BPD matter? The real goal in preventing BPD or at least minimizing respiratory morbidity of any kind is to ensure that after discharge from the NICU we are sending out the healthiest babies we can into the community. Does a baby at 36 weeks and one day free of O2 and other support have a high risk of coming back to the hospital after discharge or might it be that those that are even older when they free of such treatments may be worse off after discharge. The longer it takes to come off support one would think, the more fragile you might be. This was the goal of an important study just published entitled Revisiting the Definition of Bronchopulmonary Dysplasia: Effect of Changing Panoply of Respiratory Support for Preterm Neonates. This work is yet another contribution to the pool of knowledge from the Canadian Neonatal Network. In short this was a retrospective cohort study of 1503 babies born at <29 weeks GA who were assessed at 18-21 months of age. The outcomes were serious respiratory morbidity defined as one of: (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 (4) being on home oxygen or continuous positive airway pressure at the time of assessment While neurosensory impairment being one of: (1) moderate to severe cerebral palsy (Gross Motor Function Classification System ≥3) (2) severe developmental delay (Bayley Scales of Infant and Toddler Development Third Edition [Bayley III] composite score <70 in either cognitive, language, or motor domains) 3) hearing aid or cochlear implant use (4) bilateral severe visual impairment What did they find? The authors looked at 6 definitions of BPD and applied examined how predictive they were of these two outcomes. The combination of oxygen and/or respiratory support at 36 weeks PMA had the greatest capacity to predict this composite outcome. It was the secondary analysis though that peaked my interest. Once the authors identified the best predictor of adverse outcome they sought to examine the same combination of respiratory support and/oxygen at gestational ages from 34 -44 weeks PMA. The question here was whether the use of an arbitrary time point of 36 weeks is actually the best number to use when looking at these longer term outcomes. Great for benchmarking but is it great for predicting outcome? It turns out the point in time with the greatest likelihood of predicting occurrence of serious respiratory morbidity is 40 weeks and not 36 weeks. Curiously, beyond 40 weeks it becomes less predictive. With respect to neurosensory impairment there is no real difference at any gestational age from 34-44 weeks PMA. From the perspective of what we tell parents these results have some significance. If they are to be believed (and this is a very large sample) then the infant who remains on O2 at 37 weeks but is off by 38 or 39 weeks will likely fair better than the baby who remains on O2 or support at 40 weeks. It also means that the risk of neurosensory impairment is largely set in place if the infant born at < 29 weeks remains on O2 or support beyond 33 weeks. Should this surprise us? Maybe not. A baby who is on such support for over 5 weeks is sick and as a result the damage to the developing brain from O2 free radical damage and/or exposure to chorioamnionitis or sepsis is done. It will be interesting to see how this study shapes the way we think about BPD. From a neurosensory standpoint striving to remove the need for support by 34 weeks may be a goal worth striving for. Failure to do so though may mean that we at least have some time to reduce the risk of serious respiratory morbidity after discharge. Thank you to the CNN for putting out what I am sure will be a much discussed paper in the months to come.
  9. Earlier
  10. @hkhawahur it will be a triple-strain combination
  11. is the probiotics you are using consist of a single or more bacteria
  12. In this rather weird, but interesting study from Italy, 10 mothers of preterm babies (less than 32 weeks or less than 1500 grams) without ultrasound brain injury or severe retinopathy, and 11 mothers of full term babies were shown photos of their own baby or photos of an unknown baby (from one of the other mothers) while they had their head in an MRI magnet. (Montirosso R, et al. Greater brain response to emotional expressions of their own children in mothers of preterm infants: an fMRI study. J Perinatol. 2017). The photos were of their baby's face while happy, neutral, or crying. Using functional MRI the researchers determined the activation of several different brain areas, at 3 months corrected age. All the mothers had more activation in several areas when looking at their own baby's face than when looking at the unknown baby. When they compared the responses between the groups, the preterm mothers had greater activation in several areas both when looking at their own baby's face, and also when looking at the unknown baby's face, than the term mothers, and when viewing their own infant's face they showed increased activation in an emotion processing area (i.e., inferior frontal gyrus) and areas for social cognition (i.e., supramarginal gyrus) and affiliative behavior (i.e., insula). The mothers were reasonably well matched, and not suffering from postnatal depression or anxiety. The weeks of stress in an NICU watching their baby and being able to do little to protect them look like they change a mother's brain function. Now what about the dads? Another article (Paules C, et al. Threatened preterm labor is a risk factor for impaired cognitive development in early childhood. Am J Obstet Gynecol. 2017;216(2):157 e1- e7). and a very interesting editorial, compared 3 groups of children at 2 years corrected age. Babies born late preterm and infants who had been born at term, after an episode of preterm labour. And a group born at term, without a history of preterm labour. The groups were fairly small, (22, 23 and 42 respectively). The episode of threatened preterm labour occurred between 25 and 36 weeks gestation, and isn't described in this paper, in terms of actual gestational age or other complications associated, except that the membranes were not ruptured. Some of the mothers received steroids, and that was different between the late preterm born babies (55%) and the term delivering babies (100%). The babies born after threatened preterm labour, whether they delivered at term or late preterm had scores on the developmental/cognitive/motor function screening test which were very similar to each other in almost all domains, and also lower in almost all domains than the controls. Overall, the Odds Ratio for what they call "mild delays in development" (more than 1 standard deviation below the mean, which is really in the lower part of the normal distribution), at 2 years was about 2.0, after an episode of preterm labour. A very interesting editorial confirms that this is probably the first study to have published such outcomes, although previous studies have shown an increase in SGA after threatened preterm labour. In this new study, also, the threatened preterm labour babies born at term weighed 200 grams on average less than the controls despite being born only 1 day earlier. If this finding is true (and in such a small study we should be careful about relying on it too much) then the big question is: why? Why should an episode of threatened preterm labour, which resolves with eventual delivery at term have an effect on cerebral development? Is it an antenatal influence of perhaps increased intra-amniotic inflammation? Does such an episode affect the home environment? Is it related to the somewhat higher educational level of the control mothers? (Although this was included in the logistic regression model, the differences are quite large, 30% of term delivering babies after preterm labour only had primary education, compared to 14% of controls). If this finding is confirmed it might lead the way to further research studying the mechanisms, and help us get a handle on the impacts of preterm birth after preterm labour also.
  13. I have never been convinced that fluid restriction is a good thing for kids with BPD. I think the common practice came about because of the short-term improvements in lung function that sometimes follow if you start diuretics. The idea being that if diuretics improve lung function, then giving less fluid will also. But this is a false equivalency, diuretics cause sodium depletion, and therefore decrease total body water, and probably lung water content also. Fluid restriction in contrast leads to a reduction in urine output, and, within clinically reasonable limits, will not have an impact on total body water, and there is no reason to believe that they will reduce lung water content either. Diuretics may have other direct effects on pulmonary function, that will not occur with fluid restriction. Inhaled furosemide, for example, improves pulmonary mechanics in BPD, presumably by acting on the same sort of ion pump that loop diuretics block in the kidney. Even in adults with fluid overload (those with oedematous congestive heart failure) RCTs of fluid restricion show no effect, unless sodium intake is also severely restricted. Sodium restriction alone works as well, so the fluid restriction adds nothing. Despite this, there are recommendations from usually reliable people that babies with BPD should have their fluid intake restricted, such recommendations are often accompanied by a reference, usually a reference to another recommendation or to a narrative-type review article. I have been planning for years to do a systematic review for the Cochrane library, of fluid restriction as treatment for early or established BPD. We have finally finished the review and it has just appeared. (Barrington KJ, Fortin-Pellerin E, Pennaforte T. Fluid restriction for treatment of preterm infants with chronic lung disease. Cochrane Database of Systematic Reviews. 2017(2).) Using the usual search procedures we could only find one relevant trial. In fact the initial search didn't find the article (Fewtrell MS, et al. Randomized trial of high nutrient density formula versus standard formula in chronic lung disease. Acta Paediatrica. 1997;86(6):577-82.) even though I knew it existed; the Pubmed key words did not mention fluid volumes or restriction, so we tweaked the search to ensure that we found the article, and to make sure that we would find any others that exist. So the only RCT evidence addressing fluid restriction is a study of 60 preterm babies with early chronic lung disease (needing oxygen at 28 days of age) who were randomized to either get 180 mL/kg/day of a regular formula, or 145 mL/kg/d of a concentrated formula. Unfortunately they didn't report on one of our outcomes, oxygen requirement at 36 weeks, as it wasn't the standard outcome that it has since become. That study showed no benefit of fluid restriction on any outcome. The fluid restricted group had more apneas, a finding unlikely to be due to chance, and also had more babies who needed more than 30% oxygen during the trial, a difference which may have been due to chance. Fluid restriction risks nutritional restriction also; even though the idea may be to reduce the free water intake, babies often get fewer calories and less protein when fluid restricted, while babies with BPD actually need more calories. They will also produce more concentrated urine, which might increase the risk of nephroclacinosis as well. The final message is that there is no evidence to support the practice of fluid restriction of babies with early or established BPD. There is no physiologic rationale either. There are potential risks to the practice. We should stop doing it.
  14. @R. Hentschel the strain combination is not 100% set, but I will post info when it is. Re emails I have updated your notifications , please also have a look in your profile https://99nicu.org/notifications/options/ and you can fine-tine your notifications there.
  15. Sounds interesting. Can you supply me with information about the ingredients? And one comment: Not a further newsletter, please. My email account is full of it.
  16. Thank you for your response and very useful information
  17. Explore MPROvE's comprehensive online delivery platform for online neonatal education, videos on procedural skill training, human factors training, and technology enhanced learning: 50 videos with an evidence based approach to a variety of topics in neonatal medicine, neonatal procedural skills , protocols and reference works. The homepage provides search and browse options based on playlists covering various topics as well as a comprehensive library of videos on each topic.
  18. Dose & administration Three doses at 24-hour intervals, as intravenous injections over 15 minutes, or by oro-gastric administration: 1st dose: 10 mg/kg 2nd and 3rd dose: 5 mg/kg Indications Closure of the patent ductus arteriosus. Contraindications and special considerations (incl incompatibilities) Contraindications include: duct-dependent cardiovascular malformation active bleeding, including intracranial, gastrointestinal or lung bleeding necrotizing enterocolitis (confirmed or suspected) significant thrombocytopenia or coagulation defects significantly reduced renal function significant hyperbilirubinemia Pulmonary hypertension has been reported when ibuprofen was given within 6 hours after birth. Concomitant use the following pharmaceuticals products is not recommended: diuretics: ibuprofen may reduce the effect of diuretics, and diuretics may increase the risk of renal insufficiency in dehydrated patients. anticoagulants: ibuprofen may inhibit platelet function and concomitant use with anticoagulants may increase the risk of bleeding corticosteroids: concomitant use with ibuprofen may increase the risk of gastrointestinal bleeding nitric oxide: since both nitric oxide and ibuprofen inhibit platelet function, concomitant use may in theory increase the risk of bleeding other NSAIDs: concomitant use of more than one NSAID should be avoided because of the increased risk of adverse reactions aminoglycosides: ibuprofen may reduce clearance of aminoglycosides, concomitant use may increase the risk of nephrotoxicity and ototoxicity, and surveillance of serum levels of aminoglycides should be performed Ibuprofen should not be administrated with any acidic solution. Adverse effects Oligura and transient renal insufficiency. Ibuprofen has less renal side-effects than indomethacin. Pharmacological aspects Ibuprofen is an anti-inflammatory drug (NSAID) that reduces the synthesis of prostaglandins through a non-selective inhibition of cyclo-oxygenase. Prostaglandins are involved in the persistence of the ductus arteriosus after birth, through relaxation of the muscle layer of the ductus arteriosus. The reduction of prostaglandins by ibuprofen is believed to be the main mechanism of action. The estimated T1/2 is 30 (16-43) hours. References Summary of product characteristics. Pedea -EMEA/H/C/000549 -IG/392. (URL) Ibuprofen for the treatment of patent ductus arteriosus in preterm or low birth weight infants. Cochrane Database of Systematic Reviews 2015, Issue 2. Art. No.: CD003481. 
PMID: 25692606 Pulmonary hypertension after ibuprofen prophylaxis in very preterm infants. Lancet 2002; 359: 1486–88. PMID: 11988250 Document version history 2017-02-10 / Stefan Johansson
  19. REQUESTING THE HELP OF OTHERS TO LOOK AT SYSTEMS FOR INFUSION PRACTICES IN THE NICU. THE MESSAGE BELOW IS FROM OUR PHARMD. iF YOU ARE INTERESTED IN HELPING, SEE THE MESSAGE BELOW: Dr Scott Denne and two of our Clinical Pharmacists are investigating current NICU IV infusion practices around the country. We hope to quantify drug delivery and identify the optimal tubing/needleless component configurations for neonatal IV drug therapy. Recent background information around issues in neonatal IV drug therapy can be found here. http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm518049.htm Please ask one of your experienced nurses to follow the surveymonkey link below and provide the needed information within the next 2 weeks. Thank you very much in advance for your time. All reported information will be de-identified. https://www.surveymonkey.com/r/SMP8R5D William Buss, Pharm.D. NICU Clinical Pharmacist Riley Hospital for Children Indiana University Health
  20. The product (-s) will be available within EU28 in the first step, then global availability. We nourish big plans
  21. I also recommend Keith Barrington's comment in his blog on erythropoietin in asphyxia https://neonatalresearch.org/2016/05/09/erythropoietin-for-asphyxia/ It is about the most recent phase II study on this topic published last year.
  22. Well done! Will the products only be available in Sweden?
  23. Positive pressure ventilation puts infants at risk of developing chronic lung disease (CLD). Chronic lung disease in turn has been linked many times over, as a risk for long term impacts on development. So if one could reduce the amount of positive pressure breaths administered to a neonate over the course of their hospital stay, that should reduce the risk of CLD and by extension developmental impairment. At least that is the theory. Around the start of my career in Neonatology one publication that carried a lot of weight in academic circles was the Randomized Trial of Permissive Hypercapnia in Preterm Infants which randomized 49 surfactant treated infants to either a low (35-45) or high (45-55) PCO2 target with the thought being that allowing for a higher pCO2 should mean that lower settings can be used. Lower settings on a ventilator would lead to less lung damage and therefore less CLD and in turn better outcomes. The study in question did show that the primary outcome was indeed different with almost a 75% reduction in days of ventilation and with that the era of permissive hypercapnia was born. The Cochrane Weigh in In 2001 a systematic review including this and another study concluded that there was insufficient evidence to support the strategy in terms of a benefit to death or chronic lung disease. Despite this lack of evidence and a recommendation from the Cochrane group that permissive hypercapnia be used only in the context of well designed trials the practice persisted and does so to this day in many places. A little lost in this discussion is that while the end point above was not different there may still be a benefit of shorter term ventilation. A modern cohort It would be unwise to ignore at this point that the babies of the late 90s are different that the ones in the current era. Surfactant and antenatal steroid use are much more prevalent now. Ventilation strategies have shifted to volume as opposed to pressure modes in many centres with a shift to early use of modalities such as high frequency ventilation to spare infants the potential harm of either baro or volutrauma. Back in 2015 the results of the PHELBI trial were reported Permissive hypercapnia in extremely low birthweight infants (PHELBI): a randomised controlled multicentre trial. This large trial of 359 patients randomized to a high or low target pCO2 again failed to show any difference in outcomes in terms of the big ones “death or BPD, mortality alone, ROP, or severe IVH”. What was interesting about this study was that they did not pick one unified target for pCO2 but rather set different targets as time went on reflecting that with time HCO3 rises so what matters more is maintaining a minimum pH rather than targeting a pCO2 alone which als0 reflects at least our own centre’s practice. There is a fly in the ointment here though and that is that the control group has a fault (at least in my eyes) Day of life Low Target High Target 1-3 40-50 55-65 4-6 45-55 60-70 7-14 50-60 65-75 In the original studies of permissive hypercapnia the comparison was of a persistent attempt to keep normal pCO2 vs allowing the pCO2 to drift higher. Although I may get some argument on this point, what was done in this study was to compare two permissive hypercapnia ranges to each other. If it is generally accepted that a normal pCO2 is 35-45 mmHg then none of these ranges in the low target were that at all. How did these babies do in the long run? The two year follow-up for this study was published in the last month; Neurodevelopmental outcomes of extremely low birthweight infants randomised to different PCO2 targets: the PHELBI follow-up study. At the risk of sounding repetitive the results of Bayley III developmental testing found no benefit to developmental outcome. So what can we say? There is no difference between two strategies of permissive hypercapnia with one using a higher and the other a lower threshold for pCO2. It doesn’t however address the issue well of whether targeting a normal pCO2 is better or worse although the authors conclude that it is the short term outcomes of shorter number of days on ventilation that may matter the most. The Truth is Out There I want to believe that permissive hypercapnia makes a difference. I have been using the strategy for 15 or so years already and I would like to think it wasn’t poor strategy. I continue to think it makes sense but have to admit that the impact for the average baby is likely not what it once was. Except for the smallest of infants many babies these days born at 27 or more weeks of gestation due to the benefits of antenatal steroids, surfactant and modern ventilation techniques spend few hours to days on the ventilator. Meanwhile the number of factors such chorioamniotitis, early and late onset sepsis and genetic predisposition affect the risks for CLD to a great degree in the modern era. Not that they weren’t at play before but their influence in a period of more gentle ventilation may have a greater impact now. That so many factors contribute to the development of CLD the actual effect of permissive hypercapnia may in fact not be what it once was. What is not disputed though is that the amount of time on a ventilator when needed is less when the strategy is used. Let us not discount the impact of that benefit as ask any parent if that outcome is of importance to them and you will have your answer. So has permissive hypercapnia failed to deliver? The answer in terms of the long term outcomes that hospitals use to benchmark against one and other may be yes. The answer from the perspective of the baby and family and at least this Neonatologist is no.
  24. No worries! We find someone
  25. Most of my colleagues / friends are private practitioners and not in to academic or write ups....Sorry for the same. Regards, Mallikarjuna
  26. @Francesco Cardona @Mallikarjun we should have them all in our Pharmacopedia do you happen to know someone who would be interested to write some posts (like your nearest fellow or so)?
  27. Great link @Stefan Johansson!
  28. Thanks for the post. Inotropes are really simplified...!
  1. Load more activity
  • Who's Online   1 Member, 0 Anonymous, 18 Guests (See full list)

  • Member Statistics

    Total Members
    Most Online
    Newest Member