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Showing content with the highest reputation since 10/21/2013 in Blog Entries

  1. It has to be one of the most common questions you will hear uttered in the NICU. What were the cord gases? You have a sick infant in front of you and because we are human and like everything to fit into a nicely packaged box we feel a sense of relief when we are told the cord gases are indeed poor. The congruence fits with our expectation and that makes us feel as if we understand how this baby in front of us looks the way they do. Take the following case though and think about how you feel after reading it. A term infant is born after fetal distress (late deceleration to as low as 50 BPM) is noted on the fetal monitor. The infant is born flat with no heart rate and after five minutes one is detected. By this point the infant has received chest compressions and epinephrine twice via the endotracheal tube. The cord gases are run as the baby is heading off to the NICU for admission and low and behold you get the following results back; pH 7.21, pCO2 61, HCO3 23, lactate 3.5. You find yourself looking at the infant and scratching your head wondering how the baby in front of you that has left you moist with perspiration looks as bad as they do when the tried and true cord gas seems to be betraying you. To make matters worse at one hour of age you get the following result back; pH 6.99, pCO2 55, HCO3 5, lactate 15. Which do you believe? Is there something wrong with the blood gas analyzer? How Common Is This Situation You seem to have an asphyxiated infant but the cord gas isn’t following what you expect as shouldn’t it be low due to the fetal distress that was clearly present? It turns out, a normal or mildly abnormal cord gas may be found in asphyxiated infants just as commonly as what you might expect. In 2012 Yeh P et al looked at this issue in their paper The relationship between umbilical cord arterial pH and serious adverse neonatal outcome: analysis of 51,519 consecutive validated samples. The authors sampled a very large number of babies over a near 20 year period to come up with a sample of 51519 babies and sought to pair the results with what they knew of the outcome for each baby. This is where things get interesting. When looking at the outcome of encephalopathy with seizures and/or death you will note that only 21.71% of the babies with this outcome had a gas under 7.00. If you include those under 7.10 as still being significantly distressed then this percentage rises to 34.21%. In other words almost 66% of babies who have HIE with seizures and/or death have a arterial cord pH above 7.1! The authors did not look at encephalopathy without seizures but these are the worst infants and almost 2/3 have a cord gas that you wouldn’t much as glance at and say “looks fine” How do we reconcile this? The answer lies in the fetal circulation. When an fetus is severely stressed, anaerobic metabolism takes over and produces lactic acid and the metabolic acidosis that we come to expect. For the metabolites to get to the umbilcal artery they must leave the fetal tissues and enter the circulation. If the flow of blood through these tissues is quite poor in the setting of compromised myocardial contractility the acids sit in the tissues. The blood that is therefore sitting in the cord at the time of sampling actually represents blood that was sent to the placenta “when times were good”. When the baby is delivered and we do our job of resuscitating the circulation that is restored then drives the lactic acid into the blood stream and consumes the buffering HCO3 leading to the more typical gases we are accustomed to seeing and reestablishing the congruence our brains so desire. This in fact forms the basis for most HIE protocols which includes a requirement of a cord gas OR arterial blood gas in the first hour of life with a pH < 7.00. Acidosis May Be Good For the Fetus To bend your mind just a little further, animal evidence suggests that those fetuses who develop acidosis may benefit from the same and be at an advantage over those infants who don’t get acidemia. Laptook AR et al published Effects of lactic acid infusions and pH on cerebral blood flow and metabolism. In this study of piglets, infusion of lactic acid improved cerebral blood flow. I would suggest improvement in cerebral blood flow of the stressed fetus would be a good thing. Additionally we know that lactate may be used by the fetus as additional metabolic fuel for the brain which under stress would be another benefit. Finally the acidemic fetus is able to offload O2 to the tissues via the Bohr effect. In case you have forgotten this phenomenon, it is the tendency for oxygen to more readily sever its tie to hemoglobin and move into the tissues. I hope you have found this as interesting as I have in writing it. The next time you see a good cord gas in a depressed infant, pause for a few seconds and ask yourself is this really a good or a bad thing?
    7 points
  2. It’s been some time since I last posted here. Many things have changed in my life since then- the most important transition being my decision to move to Finland to work as a research fellow with the Baby-friendly Ventilation Study Group in Turku. The life of a beginning clinical researcher deserves a separate post here (it may even come at some point). To celebrate my first anniversary in Finland I would like to share 3 things I wish somebody had told me before I moved here. Enjoy! 1.Get nylon pants. The weather in Finland is truly whimsical. We have had a kind spring, warm summer, and lovely, colorful autumn. I was able to enjoy each of these seasons, biking in the Archipelago, watching sun that never sets, traveling north to see ruska, and finally seeing Northern Lights for the first time in my life. My only concern here is rain. It doesn’t follow laws of gravity AT ALL. How is that possible, that those raindrops are not falling DOWN from the sky, but they are literally attacking you from every direction? It took me some time to overcome my frustration and find a solution. I have closely observed (relatively) happy Finns and discovered that the most important clothing item here is… nylon waterproof pants. The trick is they have to be big enough that you can pull them over your regular pants to keep you dry and warm when it rains. This small thing has definitely improved my comfort here. It has also created that precious feeling of belongingness- I could finally proudly join the rustling and swishing sisterhood of waterproof pants. 2. Drop in the fertility rate is a real thing. Ok, I am a doctor and I KNOW it is a real thing. I know that statistics don’t lie. I know. But I kind of didn’t want to acknowledge that it may actually impact my study. We have had a fairly good start of the patient recruitment, which had kept me busy in spring. But then summer had arrived, and the recruitment slowed down. I kept thinking that maybe it’s just because of the summertime in general (like preemies would be able to pick a season when they want to arrive early, right?). But then autumn has come, and it was time to face the music- I have a problem. In order to recruit the desired number of infants, I may either stay here forever OR I need to come up with a clever solution very soon. Thankfully, I have amazingly supportive supervisors here and we decided- we are expanding! That means more traveling for me (and possibly more blog posts for you)! 3. Compulsive talking about 99nicu may help you to dance more salsa. That statement may seem rather weird, but there is a logical explanation. Very recently I’ve had a chance to attend a regional neonatal meeting in Finland. I was asked to present highlights from the 99nicu Meetup in Copenhagen. Since I like the whole concept of 99nicu.org and loved two conferences I had attended, I took that task very seriously- meticulously prepared my PowerPoint presentation and practiced my performance out loud at home. I decided to tell participants about lectures I remembered the best- neonatal transports, simulations in the NICU and infants surviving at the limit of viability. You may argue that there were more important lectures there, but those were the ones that still “spark joy” after all these months. Do you remember that sim scenario of postpartum seizures in a birthing pool that Ruth Gottstein talked about? I’ve discussed it with so many people in so many places already, that it might have become my favorite topic of random conversations with strangers. Anyways, I think the presentation went well- participants awarded me the prize for the best presentation of the evening! I received a gift card that I can use for cultural or fitness activities in Turku- including more salsa classes in my favorite dance school. Voila! Thank you 99nicu!
    6 points
  3. Our tiny babies have very tiny tracheas. So far you are probably all with me. Putting that tube in the right position is therefore tricky. In particular avoiding the right mainstem bronchus, which is the wrong position, is important. So first of all; where should the tip be? That seems obvious, it should be in the trachea, high enough above the carina that the tube never slips into the carina, but low enough that it doesn't slip out. On a plain AP radiograph, however, it isn't always clear exactly where the tube tip should be. In general ,studies have suggested that on the radiograph the tip of the tube should be T1-T2. That is based on studies where the position was directly observed, such as in post-mortem studies, and compared with an X-ray. A study from 7 years ago (Thayyil S, et al: Optimal endotracheal tube tip position in extremely premature infants. American journal of perinatology 2008, 25(1):13-16.) noted that babies who had a tube tip lower than T1-T2 were more likely to have right upper lobe collapse, localized PIE and pneumothorax. I think that confirms that T1-T2 is the appropriate location. Now how do we ensure that the tube tip is in that, optimal, position? The NRP (which clearly is not focussed on very preterm babies) suggests to add 6 cm to the infants weight in kg, which leads to tube insertion depths which are too low for most babies under 1 kg (see for example : Peterson J, et al: Accuracy of the 7-8-9 Rule for endotracheal tube placement in the neonate. J Perinatol 2006, 26(6):333-336.) I think it is clear we should not use that rule for babies under 1 kg. Various methods of calculation have been suggested, some are based on calculations using the babies weight, some on gestation, one on foot length (which actually seems to be a good idea, and relatively easy to get to during resuscitation, but I don't know if anyone does that. Embleton ND, et al: Foot length, an accurate predictor of nasotracheal tube length in neonates. Archives of Disease in Childhood - Fetal and Neonatal Edition 2001, 85(1):F60-F64) maybe Nick Embleton will let me know if anyone uses it. A newly published trial from Colm O'Donnel in Dublin (Flinn AM, et al: Estimating the Endotracheal Tube Insertion Depth in Newborns Using Weight or Gestation: A Randomised Trial. Neonatology 2015, 107(3):167-172.) randomly compared weight and gestational age based standards, unfortunately the weight based standard they used was depth= weight + 6, and they compared this to a table based on gestational age. The number of ET tubes in the right place was higher with the weight calculation, but it was not statistically significant, and there were very many that were malpositioned in both groups, 50% with the weight based calculation, and 60% with the GA table. Another study, which also trashed the 7-8-9 rule promoted by NRP, (Kempley ST, et al: Endotracheal tube length for neonatal intubation. Resuscitation 2008, 77(3):369-373) was a report of a quality improvement initiative in London. It is interesting in part because they showed that intubating the baby and then doing a clinical exam to see if it was in the right place was associated with more than half of the ETTs being mal-positioned. While using a table of distances (either GA based or weight based) was much better, with less than 20% needing repositioning. Colm O'Donnell has also published a letter with photos of endotracheal tubes (Gill I, O'Donnell CP: Vocal cord guides on neonatal endotracheal tubes. Archives of disease in childhood Fetal and neonatal edition 2014, 99(4):F344.) which clearly shows that you can't rely on the ETT marks to decide where to put the tube. Non-one ever evaluated this previously, as far as I can tell in the literature, but using those marks will lead to many being in the wrong place. I think it should be obvious that all babies who are intubated with a 2.5 tube do not have the same length of trachea! So using the same ETT tube marking wll often be wrong. So how best to do this? I think that the first step should be to use a table of insertion depth against body weight. (we are a center which attracts a lot of extremely growth restricted babies, so I would be wary of using a GA standard). I think the table below looks to be the best (the table below is from the study which I refer to above by Stephen Kempley) , I have added a column for nasal intubation based on the demonstration (autopsy study,with body weights down to 500 g) that the distance from nostril to carina is almost exactly 1.2 cm on average longer than the distance from lip to carina (Rotschild A, Chitayat D: Optimal Positioning of Endotracheal Tubes for Ventilation of Preterm Infants. AJDC 1991, 145:1007.) During the intubation procedure, prior to fixing the tube, palpation in the supra-sternal notch can confirm good tube position with very good accuracy, once you have been trained to do it. A randomized trial from Neil Finer's group (Jain A, et al: A randomized trial of suprasternal palpation to determine endotracheal tube position in neonates. Resuscitation 2004, 60(3):297-302.) who showed me the technique when I was his fellow) found a much higher proportion of tubes in the right position after adequate training, and another RCT (Saboo AR, et al: Digital palpation of endotracheal tube tip as a method of confirming endotracheal tube position in neonates: an open-label, three-armed randomized controlled trial. Pediatric Anesthesia 2013, 23(10):934-939) had a high proportion of tubes in good position, 83%, following a process such as I have just described, a table of insertion depths, accompanied by palpation to validate position. Here is that table: (sorry but I can't figure out how to make this table a good size, so click on it to view.). ((This is the initial length to which the tube should be inserted, followed by palpation of the tube to ensure good position, and then a chest radiograph to check its position. The tube length should then be adjusted to align its tip with the thoracic vertebrae T1–T2.)) Another important point, flexion of the neck advances the end of the ETT, but, in fact, the sze of the effect is fairly minor. A severe flexion of 55 degrees only advances the tube tip by about 3 mm (Rost JR, Frush DP, Auten RL: Effect of neck position on endotracheal tube location in low birth weight infants. Pediatric Pulmonology 1999, 27(3):199-202). So if the tube is on the carina when you do the x-ray and the head is flexed, you still need to reposition the tube, you can't rely on good head position to move the tube tip up much. Finally there are some data to support using ultrasound to confirm tube position, (Chowdhry R, Dangman B, Pinheiro JM: The concordance of ultrasound technique versus X-ray to confirm endotracheal tube position in neonates. J Perinatol 2015. Dennington D, Vali P, Finer NN, Kim JH: Ultrasound confirmation of endotracheal tube position in neonates. Neonatology 2012, 102(3):185-189.) It looks like this could be a reliable way of identifying malposition of the tube, and we should consider maybe training everyone to do this, including me!
    6 points
  4. The professional communication during the Covid-19 pandemic really shows the potential to share expertise and experience through web-based channels. Journals, societies, regular news media, social media platforms etc-etc play an important role for us to keep updated, and many web sites have also opened up their content free of charge. We will learn many things from facing and tackling this pandemic, but one major change will certainly be our communication channels. Many are discovering the web-based possibilities to learn and discuss. We will do our best to facilitate professional communication within the neonatal community. And, finally it seems that the company providing our software (IPB) will finally roll out a smartphone app. Which means that 99nicu will literally become available in your pocket through a "99nicu App". The screen shots below comes from the beta-version of the app now used by the company providing our software. And yes, there will be light-mode and dark-mode Stay tuned!
    5 points
  5. I must admit that it is a bit exciting to think about that 99nicu.org went live 12 years ago, at a time when Facebook and other “social media” web sites was yet to be invented. (@Zuckerberg, no offense here. Obviously, you created something far greater than 99nicu, still a grass rot project. BTW – could we apply for funding from you Foundation?) When starting 99nicu.org in 2006, we nourished an idea that experiences and expertise should not be hindered by geographical boundaries. In some sense, this was a statement, that we as medical professionals could help each other through other channels than journals and conferences, with inclusive and open mindsets, and new technologies. Back then we knew little about the powerful potential of the Internet. Neither could we foresee how the Internet would change our private and professional lives. We were just a group of young staff in Sweden, wanting to create a web based platform for discussions within a global group of neonatal pro’s. When I read this blog post by @AllThingsNeonatal (on his web site allthingsneonatal.com) where he reflects on how sharing and caring in social media has created a global village, I am struck by the thought - a global village was what we envisioned back in 2006. Coming from a small village myself, I think that also 99nicu.org parallells the village symbolism: a setting with small communication gaps (everyone knows everything about everyone, so we don't need formalities to get in touch and speak out), and where giving and taking advice is a bilateral process that may ultimately lead to “the best solution”. Or simply, that we find out that there are several good solutions for a given problem. Has 99nicu become as global village for neonatal staff on the Internet? Although biased, I’d say YES . Data also supports that. During January through April, the web site had 18.000 visitors from all over the globe, making 45.200 pageviews. From the Google Analytics dashboard we can all see that 99nicu reaches almost every corner of the world! Our principal idea has always been that the virtual space is where we operate. It is the Internet that creates the possibility to connect and exchange experience as expertise from where we are. However, meeting up IRL is also a powerful way to maintain sustainable networks and that idea is the driving force behind the “99nicu Meetups”. For the 1st and 2nd Meetup conferences in Stockholm and Vienna (in June 2017 and in April 2018), delegates came from 17 and 33 countries, respectively. Let’s hope we can have even a larger geographical representation at our IRL Meetup next year. Stay tuned for dates and location
    5 points
  6. I just want to share some brief news about our next Meetup, 7-10 April 2019 at Rigshospitalet in Copenhagen/Denmark. We (i.e myself, @Francesco Cardona @RasmusR @Christian Heiring , Gorm Greisen and Morten Breindahl) are currently working on the program lectures and workshops. I just want to share the first five confirmed speakers and their topics: Morten Breindahl: Neonatal transports – how to do them safe and easy Ola Andersson: Cord Clamping, 1.0 and 2.0 Ravi Patel: How to explain when NEC rates persist – even when a NICU does everything “Right” Ulrika Ådén: Infants surviving at the limit of viability, what are the outcomes? What shall we do? Gorm Greisen: Ethical decision making around the limit of viability- lessons from Scandinavia I'll update you all with more names and topics as they are confirmed Looking forward to meet up in Copenhagen!
    5 points
  7. The lungs of a preterm infant are so fragile that over time pressure limited time cycled ventilation has given way to volume guaranteed (VG) or at least measured breaths. It really hasn’t been that long that this has been in vogue. As a fellow I moved from one program that only used VG modes to another program where VG may as well have been a four letter word. With time and some good research it has become evident that minimizing excessive tidal volumes by controlling the volume provided with each breath is the way to go in the NICU and was the subject of a Cochrane review entitled Volume-targeted versus pressure-limited ventilation in neonates. In case you missed it, the highlights are that neonates ventilated with volume instead of pressure limits had reduced rates of: death or BPD pneumothoraces hypocarbia severe cranial ultrasound pathologies duration of ventilation These are all outcomes that matter greatly but the question is would starting this approach earlier make an even bigger difference? Volume Ventilation In The Delivery Room I was taught a long time ago that overdistending the lungs of an ELBW in the first few breaths can make the difference between a baby who extubates quickly and one who goes onto have terribly scarred lungs and a reliance on ventilation for a protracted period of time. How do we ventilate the newborn though? Some use a self inflating bag, others an anaesthesia bag and still others a t-piece resuscitator. In each case one either attempts to deliver a PIP using the sensitivity of their hand or sets a pressure as with a t-piece resuscitator and hopes that the delivered volume gets into the lungs. The question though is how much are we giving when we do that? High or Low – Does it make a difference to rates of IVH? One of my favourite groups in Edmonton recently published the following paper; Impact of delivered tidal volume on the occurrence of intraventricular haemorrhage in preterm infants during positive pressure ventilation in the delivery room. This prospective study used a t-piece resuscitator with a flow sensor attached that was able to calculate the volume of each breath delivered over 120 seconds to babies born at < 29 weeks who required support for that duration. In each case the pressure was set at 24 for PIP and +6 for PEEP. The question on the authors’ minds was that all other things being equal (baseline characteristics of the two groups were the same) would 41 infants given a mean volume < 6 ml/kg have less IVH compared to the larger group of 124 with a mean Vt of > 6 ml/kg. Before getting into the results, the median numbers for each group were 5.3 and 8.7 mL/kg respectively for the low and high groups. The higher group having a median quite different than the mean suggests the distribution of values was skewed to the left meaning a greater number of babies were ventilated with lower values but that some ones with higher values dragged the median up. Results IVH < 6 mL/kg > 6 ml/kg p 1 5% 48% 2 2% 13% 3 0 5% 4 5% 35% Grade 3 or 4 6% 27% 0.01 All grades 12% 51% 0.008 Let’s be fair though and acknowledge that much can happen from the time a patient leaves the delivery room until the time of their head ultrasounds. The authors did a reasonable job though of accounting for these things by looking at such variables as NIRS cerebral oxygenation readings, blood pressures, rates of prophylactic indomethacin use all of which might be expected to influence rates of IVH and none were different. The message regardless from this study is that excessive tidal volume delivered after delivery is likely harmful. The problem now is what to do about it? The Quandry Unless I am mistaken there isn’t a volume regulated bag-mask device that we can turn to to control delivered tidal volume. Given that all the babies were treated the same with the same pressures I have to believe that the babies with stiffer lungs responded less in terms of lung expansion so in essence the worse the baby, the better they did in the long run at least from the IVH standpoint. The babies with the more compliant lungs may have suffered from being “too good”. Getting a good seal and providing good breaths with a BVM takes a lot of skill and practice. This is why the t-piece resuscitator grew in popularity so quickly. If you can turn a couple dials and place it over the mouth and nose of a baby you can ventilate a newborn. The challenge though is that there is no feedback. How much volume are you giving when you start with the same settings for everyone? What may seem easy is actually quite complicated in terms of knowing what we are truly delivering to the patient. I would put to you that someone far smarter than I needs to develop a commercially available BVM device with real time feedback on delivered volume rather than pressure. Being able to adjust our pressure settings whether they be manual or set on a device is needed and fast! Perhaps someone reading this might whisper in the ear of an engineer somewhere and figure out how to do this in a device that is low enough cost for everyday use.
    5 points
  8. Originally posted at: https://winnipegneonatal.wordpress.com/ Facebook Page: https://www.facebook.com/allthingsneonatal/ As I read through the new NRP recommendations and began posting interesting points on my Facebook Page I came across a section which has left me a little uneasy. With respect to a newborn 36 weeks and above who is born asystolic and by ten minutes of age continues to remain so and has an apgar score of zero the recommendation that has been put forward is this: An Apgar score of 0 at 10 minutes is a strong predictor of mortality and morbidity in late-preterm and term infants. We suggest that, in babies with an Apgar score of 0 after 10 minutes of resuscitation, if the heart rate remains undetectable, it may be reasonable to stop resuscitation; however, the decision to continue or discontinue resuscitative efforts should be individualized. Variables to be considered may include whether the resuscitation was considered to be optimal, availability of advanced neonatal care, such as therapeutic hypothermia, specific circumstances before delivery (eg, known timing of the insult), and wishes expressed by the family (weak recommendation, very-low-quality evidence). There are some significant problems with this part of the statement. They claim that the apgar score at ten minutes is a strong predictor but when you look at the analysis of the evidence presented in the body of the paper it is weak at best. I am not clear how one declares the prediction is strong in the face of poor evidence but I will acknowledge intuitively that this makes some sense but do challenge them on the use of the word "strong". 2. They are correct in acknowledging that the introduction of hypothermia in such settings has changed the landscape in as much as I find it quite difficult to prognosticate unless a child is truly moribund after resuscitation. Given such uncertainty it is concerning to me that this recommendation may be committed to memory incorrectly in some places that do have access to cooling and may be used more rigidly as though shalt stop at 10 minutes. 3. In the middle of a resuscitation it is quite difficult to process all of the facts pertaining to a particular newborn while orders for chest compressions, emergency UVCs and epinephrine are being given. Can we really individualize within ten minutes accurately and take the families wishes truly into account? This just does not seem practical. 4. The families wishes are taken into account but inserted as a "weak recommendation". How can the wishes of the family in any family centred model of care be minimized in such a way even if we believe the situation to be dire? 5. Since the introduction of hypothermia there appears to be a near 50% survival rate in such newborns and as the authors state 27% of survivors who received cooling had no moderate or severe disability. Here in lies my greatest issue with this guideline and that is the hypocrisy this position takes when you compare populations at 23 and 24 weeks gestational age. Survival at these GA in the recent NEJM study of almost 5000 preterm infants under 27 weeks were 33 and 57 % respectively at 23 & 24 weeks with rates of survival without moderate or severe disability being 16 and 31% in the two groups. The fallout from this and other studies at the extremes of gestational age have been that we should be more aggressive as the outcomes are not as bad as one would predict. How can we argue this for the 23-24 week infants and for term infant with the same likelihood of outcomes we would unilaterally stop in many centres?! So Now What Do We Do? We are supposed to be practising family centred care and much like the argument at the edge of viability the same should apply here. The wishes of the family should never be minimized. Arguably it may be very difficult in such an unexpected scenario to appraise a family of the situation and have clarity around the issue but if a heart rate can be restored after a few more minutes do we not owe it to the family and the child to bring the infant back to the NICU and see what transpires especially if cooling is available? The million dollar question of course is where do we draw the line? No heart rate at 15, 20 minutes? Based on the evidence thus far it seems to me that a little longer than 10 minutes is reasonable especially in well equipped centres with access to cooling and modern ventilation and treatments for pulmonary hypertension. How long though must be individualized and should be determined in partnership with the team caring for the patient which must include the family.
    5 points
  9. Intubate-Surfactant- Extubate or INSURE has been around for awhile. The concept is to place an ETT while an infant is first on CPAP and then after pushing surfactant in quickly remove the ETT and put back on CPAP. This does not always go as planned though. If after surfactant the FiO2 remains above 30% many people would keep the ETT in place as they would surmise that the infant would fail if the tube was removed. They would probably be right. Sustained inflations have fallen out of favour ever since the SAIL trial results were published and written about here . Having said that, the concept of using sustained inflation is to open the lung and expand closed alveoli to improve both oxygenation and gas exchange. Much like giving inhale nitric oxide to a collapsed lung is unlikely to make much difference, the question could be asked whether giving surfactant to a lung that is most collapsed will fail to deliver this compliance improving medication to the areas of the lung that most sorely need it. Our Italian colleagues therefore decided to undertake a study to look at providing surfactant to lungs after a recruitment manouver and see if this made a difference to the meaningful outcome of extubation failure after surfactant provision. The results are intriguing and as such here we go in looking at the study. Optimizing Lung Expansion The trial is the Lung recruitment before surfactant administration in extremely preterm neonates with respiratory distress syndrome (IN-REC-SUR-E): a randomised, unblinded, controlled trial and involved 35 NICUs in Italy. All infants enrolled were born from 24 + 0 weeks to 27 6/7 weeks gestational age at birth and all < 24 hours of age at enrollment. Each baby had to be on CPAP at the time of randomization and meet prespecified failure criteria of FiO2 of 0·30 or greater for target SpO2 of 87% to 94% for at least 30 min or in 10 Infants for rapid deterioration of clinical status or if pCO2 was > 65 mm Hg with a pH less than 7·20. Regardless of which arm they were randomized to all infants received 1-2 sustained inflation breaths using 25 cm H2O for 10-15 secs using a t-piece resuscitator after being started on CPAP as was the practice at the time. After randomization which could not be blinded, patients were then either given surfactant via INSURE without any further strategy for opening the lung or received the IN-REC-SUR-E approach. The latter involved putting the infant on high frequency oscillation starting with settings of mean airway pressure 8 cm H2O; frequency 15 Hz; ΔP15 cm H2O; and inspiration to expiration ratio of 1:2. Using this modality infants underwent stepwise recruitment methods prior to administering surfactant (poractant). The primary outome was the need for mechanical ventilation within the first 72 h of life. Infants met the primary outcome if they were not extubated within 30 min after surfactant administration or required reintubation before 72 h of life. The Results Based on a power calculation the authors needed 103 infants in each arm and they recruited 107 in the treatment and 111 in the control arm. In the per-protcol allocation 101 received the treatment and 111 the contol. While the strategies for extubation were not set out to be equal (units were allowed to extubate to anywhere from +6 to +8 for pressure levels), the groups were not different 7·0 cm H2O, SD 0·4 for the experimental group and control arms. Given the steps taken to open the lung in the lung recruitment arm, the FiO2 was lower at 28% prior to surfactant provision in the treatment group than in the usual INSURE approach at 42% prior to surfactant provision. All infants were extubated within 30 minutes of receiving surfactant. As the results demonstrate, whether there was an intention to treat analysis or per-protocol analysis the babies who received the intervention were more likely to remain extubated. The number needed to treat was 7 which is a pretty powerful measure. Interestingly, looking at secondary outcomes there are some interesting trends as well including less mortality which on a per-protocol analysis was significant but also a trend towards more PVL at 9% in the treatment arm and 4% in the control. The mean times to surfactant administration were 4 hours in the treatment group and 3 hours in the control but the high frequency manoeuvre had a mean duration of only 30 minutes. It is possible that the use of high frequency could have blown off CO2 to very low levels but I am uncertain if the short reduction in pCO2 could have contributed significantly to reduced cerebral perfusion if that trend is representative of something. Interestingly, pneumothroaces were not different between groups as no doubt as a reader you might wonder if use of high pressures to recruit the lungs when they are non compliant might have led to air leaks. So it worked, now what? First of all, the results to me make a lot of sense. Opening the lung before delivering surfactant and then seeing better chances of staying extubated doesn’t really surprise me. Some questions that come up now for me would be how this strategy would fare in those who are older at birth. I suspect given the greater chest wall support and lower likelihood of severe RDS this strategy might be even more effective at reducing FiO2 or perhaps CPAP need in terms of duration after extubation. I would think it unlikely to make a difference in reintubation though as most would remain extubated regardless. That is for another study though with a different outcome. There will be centres that don’t like the use of HFOV for recruitment so what other strategies could be used in lieu of this? I hate to say it but there will also be calls to have a much larger study specifically designed to look at the secondary outcomes. Would a larger study find a significant increase in PVL or demonstrate that it was just a random finding? Might mortality be proven to be lower and even more so? Regardless of the above what I think this paper does is give us reason to pause before giving INSURE and ask ourselves if we have done what we can to open the lung after intubating before rushing to squirt the surfactant in. Maybe increasing the provided PEEP and lowering the FiO2 somewhat before giving surfactant will help with distribution and increase your chances of first being able to extubate and secondly when you do keeping the tube out!
    4 points
  10. 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.
    4 points
  11. If you are to read one paper on neonatal ethics this year, I'd argue that this is the one. Late last year, John Lantos, pediatrician and a leading medical ethicist, published a review in NEJM on the ethics around decision-making in the NICU. The paper is not open-access... but you can surely get it from within your hospital intranet or your university/hospital library. We have a fantastic toolbox in the NICU. We can provide live-saving treatments and support. Most newborns in the NICU survive to good long-term health. However, we also operate in a high-risk environment where some infant may suffer, some infants will die, and some infants will survive with difficult sequele. Which raises the question, by staff and by parents, what is the "right" thing to do in complex situations. When withholding and withdrawing life-sustaining therapies becomes a option to decide upon. How could we navigate in this landscape? IMHO, the review by Lantos is a good starting point on how to form a local practise. Lantos shares his reasoning about we cannot "solve" these discussion with "information" as such. Despite how hard we try, data alone does not lead the whole way. Outcomes is hard to measure, they change over time and we all percieve risks differently. Therefore, information is difficult to standardize. Furthermore, those of us sharing the information will filter our presentation through our subjective selves, coping with opinions, experiences and our expertise in different ways. The better alternative around ethical questions is shared decision-making. Two central quotes of the review is that and that Certainly, the future of neonatal care will bring more ethical questions to us. Refined prenatal diagnostics, the down-shifting boundary of viability and new treatment technologies in the future (like the artificial placenta) will impact how we think about fetal life and postnatal life, what is the "periviable grey zone" and what our fantastic toolbox can do. While improving our skills, from a medical/technical viewpoint, we also need to improve how we cope with the ethics around decision-making processes. Besides reading the review by John Lantos, I can recommend you to see this lecture from theh #99nicuMeetup in Copenhagen 2019, by Eduard Verhagen. (Feature Photo : Cropped photo by Liane Metzler on Unsplash)
    4 points
  12. This has been a question that has befuddled Neonatologists for years. Get ten of us in a room and you will get a variety of responses ranging from (talking about caffeine base) 2.5 mg/kg/day to 10 mg/kg/day. We will espouse all of our reasons and question the issue of safety at higher doses but in the end do we really know? As I was speaking to a colleague in Calgary yesterday we talked about how convinced we are of our current management strategies but how we both recognize that half of what we think we know today we will be questioning in 10 years. So how convinced should we really be about caffeine? Even the Cochrane Review Suggests There Is Something Amiss Back in 2010 the Cochrane Collaboration examining 6 trials on caffeine for treating apnea of prematurity concluded “Methylxanthine is effective in reducing the number of apnoeic attacks and the use of mechanical ventilation in the two to seven days after starting treatment.” Notice the bolded section. Two to seven days. Interesting that we don’t see the effect last in perpetuity. Why might that be? Do babies become resistant with time or is there a change in the way these infants metabolize the drug such that levels in the bloodstream drop after that time point. It is almost certainly the latter and in the last 7 years have we really seen any response to this finding? I would say no for the most part although I don’t work in your unit so hard to say for sure. At least where I practice we pick a dose somewhere between 2.5-5 mg/kg/day and give a load of 10 mg/kg when we start the drug. From time to time we give a miniload of 5 mg/kg and may or may not increase the dose of maintenance based on the number of apneic events the babies are having. What if we could be proactive instead of reactive though. Do the babies need to have multiple events before we act or could we prevent the events from happening at all? Proactive Treatment With Caffeine We have known that caffeine clearance increases with postnatal age. The half-life of the drug shortens from about a week at the earliest gestational ages to 2-2.5 days by term equivalent age. For those infants who are older such as 32 weeks and above we expect them to be off caffeine (if they need it) within 2-3 weeks so I am not really talking about them but what about the babies born earlier than that or certainly MUCH earlier at 23 and 24 weeks who will be on caffeine possibly till term. Should one size (dose) fit all? No it really shouldn’t and some crafty researchers led by Koch G have published a paper that demonstrates why entitled Caffeine Citrate Dosing Adjustments to Assure Stable Caffeine Concentrations in Preterm Neonates. In this paper the authors armed with knowledge of the half life of caffeine at different gestational ages were able to calculate the clearance of the drug at different postnatal ages to demonstrate in a model of a 28 week male infant weighing 1150g. The authors further took into account predicted weight changes and were able to calculate what the expected caffeine levels would be in the fictional infant at various time points. The target caffeine levels for this patient were a trough level of 15 -20 mg/L which are the currently acceptable ranges in the literature. The testing was first done using a standard load of 10 mg/kg (base) followed by 5 mg/kg/d and demonstrated levels which yielded the following graph over time. What this demonstrates is that if the dose is unchanged over the first 7 weeks, this hypothetical infant will only achieve effective concentrations for the first week. Interesting isn’t it that the Cochrane review found clinical effect over the first 2-7 days? What if you were to double the dose to really “hit” the infant with a good dose of caffeine from the start and maintain at that level based on their weight gain as shown next. Well, you will get what you are hoping for and keep the trough level above 15 mg/L but you will hit 30 mg/L that some have said is too high and can lead to adverse effects (ever seen SVT with these high doses? I have). Like Goldilocks and the Three Bears could there be a dosing strategy that might be just right? The authors put in another model based on the knowledge of caffeine clearance over time and suggested a strategy in which after the first week the adjusted maintenance doses would be 3 mg/kg/day and 3.5 mg/kg/day in the third to fourth weeks and lastly 4 mg/kg/d in the 5th to 8th week. Using that dosing schedule the model produced this curve. As you can see, the infant would have a therapeutic target without reaching levels above 30 mg/L and potential for side effects. As many of you read this however you may ask the obvious question. Each of us have seen infants who require higher doses than this to rid themselves of significant apnea and escape reintubation. Given that this is a mathematical model it assumes that this fictional infant will respond beautifully to a trough level of 15 to 20 mg/L but some will not. Even in the curve shown it is clear that there is some room to go higher in the dosing as the curve is just touching 20 mg/L. A Suggestion For The Future What grabbed my attention here is the possibility that we could take a proactive rather than reactive approach to these infants. Once a small baby is controlled on their dose of caffeine whether it is 2.5, 3, 5 or even 6 mg/kg/d of caffeine should we wait for more events to occur and then react by increasing caffeine? What if we are too late to respond and the patient is intubated. What effect does this have on the developing lung, what about the brain that is subjected to bradycardic events with resultant drops in cardiac output and cerebral perfusion. Perhaps the solution is to work with our pharmacists and plan to increase dosing at several time points in the infants journey through the NICU even if they aren’t showing symptoms yet. No doubt this is a change in approach at least for the unit I work in but one that should start with a conversation!
    4 points
  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.
    4 points
  14. I know - many of us want less emails... But the emails from Evidence Updates are great! Evidence Updates (a collaboration project by the BMJ Group and McMaster University) assists your reading of new research by grading articles by "Relevance" and "News-worthiness". For example, this trial on D-vitamin supplementation of preterm infants showed up in an email alert, an article I had missed otherwise. 1. You need to Register (here!) 2. Choose your clinical interest ("Pediatric Neonatology", I guess) 3. Set a minimum score for new articles you want to read about (set a higher minimum score to get fewer emails ) 4. Watch your inbox! Link to like: Evidence Updates.
    4 points
  15. It is one of the first things that a medical student pledges to do; that is to do no harm. We are a fearful lot, wanting to do what is best for our patients while minimizing any pain and suffering along the way. This is an admirable goal and one which I would hope all practitioners would strive to excel at. There are times however when we can inadvertently cause more harm than good when we try to avoid what we perceive is the greater harm. This is the case when it comes to collecting a sample of urine for culture as part of a full septic workup. If you ask most healthcare providers they will freely acknowledge that the gold standard for determining whether an infant has a UTI is a supra pubic aspirate (SPA). We so rarely do them these days however due to a whole host of reasons. Problems with collection include the timing and accuracy of needle placement both of which may often lead to an empty tap. Secondly after a number of missed attempts and a crying infant who appears to be in pain it is understandable why bedside nurses may become frustrated with the entire experience and urge the person performing such procedures to settle on a bladder catheterization (BC) to obtain the specimen. The Study That Compares BC and SPA Head to Head A recent Turkish study by Eliacik K et al published A Comparison of Bladder Catheterization and Suprapubic Aspiration Methods for Urine Sample Collection From Infants With a Suspected Urinary Tract Infection and should give us all cause for concern. The authors performed SPA on 83 infants under 12 months with a positive urine culture by BC but who had not yet started antibiotics. The outcome of interest was both the comparison with the culture result and to see if urinalysis from the BC could increase the strength of the information gleaned from a BC. All in all the BC performed quite poorly when compared to the gold standard. The false positive rate compared to SPA was 71.1%! That is to say that only 28.9% of SPA samples were positive compared to BC. Similarly urinalysis sensitivity and specificity from BC were 66.7% (95% CI, 44.68% to 84.33%) and 93.22% (95% CI, 83.53% to 98.08%), respectively. This means that only 2/3 of the time was the urinalysis abnormal on a BC in the presence of a true UTI. Somewhat reassuring is that when there really was no UTI the urinalysis was mostly negative but in almost 1/10 patients it would not by itself rule out a UTI. What Is The Harm in Continuing BC Instead of SPA? When we try to avoid the perceived painful experience of a SPA we are going to wind up treating a large number of patients for a presumed UTI who don't have one. The harm in this is the exposure of such infants to prolonged courses of antibiotics which has been a subject discussed many times over on this site. We put our patients at risk of antibiotic resistance and shifts in the gut microbiome which in the case of the preterm infant puts them at risk of necrotizing enterocolitis. There are many other concerns with prolonging antibiotics but these few should be reason enough to strive for accuracy in obtaining the right specimen in the right way. Putting it in a slightly different perspective, would you settle for an alternative test to a lumbar puncture which claimed to miss 1 in 10 cases and also found meningitis where there was none 71.1% of the time?! A Way Forward - A Recipe For Success As the saying goes, measure twice and cut once. With the use of bedside ultrasound there should be no need to guess as to whether the bladder is full or not. Secondly the placement of the needle should no longer need to rely on landmarking but actually seeing where the best place for needle placement is. Assessing the bladder by ultrasound is easy and is already employed at the bedside by nurses in many areas of the hospital. There should no longer be a reason for the empty tap as the practitioner can be called when the baby is ready as evidenced by a good amount of urine in the bladder. Given that we have some time to do the blood culture and LP, while we wait for the SPA to be done either sucrose in the premature infant or IV analgesic may be given for the SPA while in the term or older infant there is an opportunity to put a topical analgesic cream over the site. There really is little need for pain to factor into this any longer. Ask any health care provider and they will tell you they want to do the best they can for their patient. This study shows us that performing a BC is failing to meet that goal. We need to change our ways and return to the practice of the SPA but this time we have to get it right.
    4 points
  16. Three recent-(ish) articles examining how we should ventilate babies and monitor what we are doing. Milner A, Murthy V, Bhat P, Fox G, Campbell ME, Milner AD, et al. Evaluation of respiratory function monitoring at the resuscitation of prematurely born infants. Eur J Pediatr. 2014:1-4. In this study, respiratory function monitoring with tidal volume, airway pressure and exhaled CO2 was routinely introduced in 2 London hospitals. The authors then asked trainees whether they found it useful, and what they thought the right tidal volume should be. As you might imagine the answers were quite variable, and integrating more than one sign, such as a lack of exhaled CO2 despite measured tidal volumes, was quite variable. van Vonderen JJ, Hooper SB, Hummler HD, Lopriore E, Te Pas AB. Effects of a Sustained Inflation in Preterm Infants at Birth. The Journal of pediatrics. 2014. Tony Milner was one of the authors of that previous article; many years ago he demonstrated that standard ventilation techniques led to an apparent 'opening pressure', where a substantial positive pressure was required to get air into the lungs, and that the end-expiratory volume of the lungs in the first few breaths remained very low. In contrast a long slow inflation (3 to 5 seconds) eliminated the opening pressure, in intubated babies, and led to establishment of an FRC. This new article used a pressure of 25 cmH2O and duration of 10 seconds, delivered by face mask, but was unable to show the establishment of an FRC, unless the babies were breathing. Murthy V, Creagh N, Peacock J, Fox G, Campbell M, Milner A, et al. Inflation times during resuscitation of preterm infants. Eur J Pediatr. 2012;171(5):843-6. This observational study during resuscitation, using the same respiratory function set up as in the first article, could not show that the variation in inflation times which occurred by chance during resuscitation (from 0.3 to 3 seconds) did not affect inspiratory flow duration. Neil Finer reviews the current state of the art of prolonged inflations, his conclusion: 'not ready for prime time'. Schilleman K, Witlox RS, van Vonderen JJ, Roegholt E, Walther FJ, te Pas AB. Auditing documentation on delivery room management using video and physiological recordings. Archives of Disease in Childhood - Fetal and Neonatal Edition. 2014. If you video record resuscitations, and then compare the tapes to what is actually written in the patients chart, this is what you get: Hmmm.. maybe we need cameras everywhere and make the recordings part of the patients chart... or maybe not!
    4 points
  17. Fantastic put together webinar by neonatal transport Seneo work neonatal transport group. Here are some favorite suggestions. 🔷Ear Muffs 🔷Air mattress 🔷Blanky with mum swell 🔷Fuzzy toy. 🔷Thank the Drivers : Be aware of G force driver have take with sudden break. 🔹Consider 🚑 design allow all to have a better transport experience. From my perspective it was Interesting the neonatal transport Landscape is diverse from the pioneering region Catalonia that NICU/PICU in 1995(🟢) to other regions that don’t. For example, Galicia have a private providers. Madrid & Valencia have dedicated Neonatal teams ( light 🔵). Some team's like the Balear region team have available helicopters/planes. Below is map showing the situation.Regions in 🛑 done by regional Emergency Teams. Benchmarking there work in a effort to improve the quality, provide constructive feedback and find ways to better ways to collaborate. Benchmarking and humanize care are interlinked with each other. They also underlined that need to keep in constant communication between the transport teams and the coordination hub.
    3 points
  18. In recent years we have moved away from measuring and reporting gastric residuals. Checking volumes and making decisions about whether to continue feeding or not just hasn’t been shown to make any difference to care. If anything it prolongs time to full feeds without any demonstrable benefits in reduction of NEC. This was shown in the last few years by Riskin et al in their paper The Impact of Routine Evaluation of Gastric Residual Volumes on the Time to Achieve Full Enteral Feeding in Preterm Infants. Nonetheless, I doubt there is a unit in the world that has not had the following situation happen. It is 2 AM and the fellow on call is notified that they need to come and see a patient. On arrival the bedside nurse shows them a syringe that contains dark green murky fluid. The fellow is told that NG tube placement was just being checked and this is what was aspirated. The infant is fine in terms of exam but the question is asked “What should I do with this fluid”. The decision is made that the fluid looks “gross” and they discard it and then decide to resume feedings with a fresh batch of milk. Both parties feel good about discarding what looked totally unappealing for anyone to ingest and the night goes on. If this sounds familiar it should as I suspect this happens frequently. Logical Fallacy A colleague of mine introduced me to this concept and I think it may apply here. Purdue University’s writing lab defines a Logical Fallacy in this way “Fallacies are common errors in reasoning that will undermine the logic of your argument. Fallacies can be either illegitimate arguments or irrelevant points, and are often identified because they lack evidence that supports their claim.” I think we may have one here that has pervaded Neonatology across the globe. Imbedded in the fallacy is the notion that because the dark green aspirates look gross and we often see such coloured aspirates in patients with necrotizing enterocolitis or other bowel disease, all green aspirates must be bad for you. The second fallacy is that the darker the aspirate the more seriously you should consider discarding it. This may surprise you but on their own there isn’t much of anything that has been shown to be wrong with them. Looking for evidence to demonstrate increased rates of NEC or other abdominal issues in an otherwise well patient finds pretty much nothing to support discarding. A challenge to discarding Athalye-Jape G et al published Composition of Coloured Gastric Residuals in Extremely Preterm Infants-A Nested Prospective Observational Study. The study was a nested one in that questions about gastric residuals were taken from two studies on the use of probiotics. As with other studies on the use of probiotics there were some benefits seen as shown in Table 2 but that is not the main reason for sharing this study with you. The main reason for the share of this paper is what is in Table 3. Although not significantly different the mean estimates for concentration of bile acids in the pale and dark green aspirates came close to being different. Other nutritional content such as fat, protein and carbohydrate were no different. As the bile became darker though the bile acids tended to increase. It is this point that is worthy of discussion. A Breakdown of the Aspirate I’m with you. When you look at that murky dark green fluid in the syringe it just seems wrong to put that back into a belly. Would you want to eat that? Absolutely not but when you break it down into what is in there, suddenly it doesn’t seem so bad. We assume that we would not want to refeed such putrid looking material and that is where the logical fallacy exists. What evidence do we have that refeeding that fluid is bad? As I said above not much at all. Looking at the fact that there is actual nutritional calories in that fluid and bile acids as well you come to realize that throwing it away may truly not be in the best interest of the baby. Calories may wind up in the garbage and along with them, bile acids. Bile acids are quite important in digestion as they help us digest fat and moreover as they enter the ileum they are reabsorbed in large quantities which go to further help digestion. In addition bile acid concentrations are what helps draw fluid into bile and promotes bile flow. By throwing these bile acids out we could see lower bile volumes and possible malabsorption from insufficient emulsification of fat. The other unmeasured factors in this fluid are the local hormones produced in the bowel such as motilin which helps with small bowel contractility. Loss of this hormone might lead to impairment of peristalsis which can lead to other problems such as bacterial overgrowth and malabsorption. Now all of this is speculative I will admit and to throw out one dark green aspirate is not going to lead to much harm I would think. What if this was systematic though over 24 or 48 hours that such aspirates were being found and discarded. Might be something there, What I do think the finding of such aspirates should trigger however is a thorough examination of the patient as dark green aspirates can be found in serious conditions such as NEC or bowel perforation. In the presence of a normal examination with or without laboratory investigations what I take from this study is that we should question are tendency to find and discard. Maybe the time has come to replace such fear with a practice of closing our eyes and putting that dark green aspirate right back where it came from.
    3 points
  19. I recently had the honour of being asked to present grand rounds at the University of Manitoba. My former Department Head during the question period stumped me when he asked me what role angiotensin converting enzyme 2 receptor (ACE2) has in pediatric COVID19. Like all great teachers, after I floundered and had to confess that while I was aware there is a role in COVID19 I wasn’t sure of the answer, he sent me a paper on the subject. The reality is that a very small percentage of COVID19 illness is found in children. Some estimates have it at 2%. Why might that be? It’s what’s in the nose that matters What has been known for some time know is that the point of entry for SARS-CoV-2 is the nasal epithelium. What is also known is that the receptor that the virus binds to in order to gain access to the host. Such binding and what happens after the virus gains entry to the body is shown in this figure depicting the life cycle of SARS-CoV-2. In a research letter by Bunyavanich et al Nasal Gene Expression of Angiotensin-Converting Enzyme 2 in Children and Adults looked at 305 patients from ages 4-60 years to examine biomarkers of asthma. In the course of looking at the nasal epithelium of these patients, they found age related differences in the expression of ACE2 receptors as shown in the following figure. I think the results somewhat speak for themselves. The younger you are the less receptors you have. If you have less receptors maybe you are less likely to contract the virus! What we don’t know This research leads to some interesting questions. Drugs such as losartan and valsartan already exist and function by blocking he ACE2 receptor. Could blockade help to limit the spread of infection? I am not aware of any such trials going on at the moment but something worth looking at. The other point that needs to be raised is that the most vulnerable group of ages >60 were not looked at in this study. The trend would certainly indicate that with age we would expect the receptor numbers to increase but since we don’t actually have the data in the older groups we don’t know if receptor numbers start to fall again with age. Similarly we don’t know below the age of 4 what receptor numbers are like. In examining risk of vertical transmission it is worth noting that the recent placental positive RT-PCRs as in Detection of SARS-COV-2 in Placental and Fetal Membrane Samples. In that study while 3 of 11 placental membranes tested positive, none of the newborns were infected. Could it be the fetus and newborn is protected by having very little density of ACE2 receptors? Something to look at and will be no doubt. Regardless, in the fight against COVID19 maybe one direction for therapeutic targeting should be addressing this receptor and seeing if there is something we can’t do to make it less susceptible to binding.
    3 points
  20. Dear fellow Ph.D. students, full-time researchers, and other fellow scientists, please #staythefuckhome. In many grant proposals, we write "this research has the potential to save lives, because... ". Let's face it- most of our research won't save lives (or at least not at once)*. No matter how fantastic our research projects are, science takes time. But what can actually save lives immediately is US STAYING HOME. This way we - the (relatively) young people in big academic campuses- won't be spreading the virus that might be deadly for others: for an old lady in the shop (who takes care of her ill husband at home), our senior supervisor (who is also an attending in the unit, so in case he gets sick, they would be running understaffed), a young mother (who will have only moderate symptoms, but will have to arrange some care for her children- possibly transferring them to her own parents, exposing them to an infection). Let's think outside of our own bubble. I don't know if there's much more we can do, but if we are lucky, it might be just enough. Work from home, write from home, think from home, read from home. We always complain that there's not enough time to read and learn- here's your chance! And if your main area of interest is neonatology, there's a fantastic treat for you- if you stay home. Karolinska NIDCAP Training and Research Center organizes a *fabulous* online conference. Go to their pages, write an email (stina.klemming@sll.se) and get your link to access this amazing event. Kind regards, Katarzyna #staythefuckhome Piatek *unless you're actually working on the vaccine or new drug for coronavirus- then just keep working ❤️
    3 points
  21. After watching a documentary in ARTE about bacteriophages it made me think about how else is antibiotic resistance in NICU.? It available french / German Here the story phages was told. First discovered use by Felix Derrel to combat infections in the pre-antibiotics era and was later discredited and forget about in the western world Historically they worked rather well, so there is an attempt to bring them back in the light of increasing antibiotics resistance. This rediscovery started with lab study that showed that the phages were effective at clearing infection in rats population sample. Phagoburn Recently, a French team took it to human and show it feasible despite the many challenges. This study was a RCT which a specific process approval and protocols were established. The aim in *Phagoburn*was to see if phages could be useful using to fight infection in burn victims. It was lead by Dr. Patrick Jault and large team .Jerôme Gabbard head Start up tells Pherecydes provided the synthesis of phages. control got standard treatment {silver salts +antiobiotics} and othe got phages.This got published in nature. The was a reduction in the infection rate in phage group, a loading dosing issue among other practical things. Researchers in france say that there a scaling issue to produce larger amounts, as well a regulatory framework. From bioethical point of view it is possible, a more detail informed consent will be necessary.These days research still going a la Croix de Lion Hospital, France. University Hospital ~CHU Lyon~. ( initial used - discovered @pasteur Institute) https://www.arte.tv/fr/videos/078693-000-A/l-incroyable-histoire-des-tueurs-de-bacteries/ Thus what do think any future of phage in NICU?
    3 points
  22. Oral immune therapy (OIT) has really taken off at least in our units. The notion here is that provision of small amounts (0.2 mL intrabucally q2or 24 hours) can prime the immune system. Lymphoid tissue present in the oropharynx and intestine exposed to this liquid gold in theory will give the immune system a boost and increase levels of IgA. Such rises in IgA could help improve the mucosal defence barrier and therefore lessen the incidence of late onset sepsis. Rodriguez et al described this in their paper Oropharyngeal administration of colostrum to extremely low birth weight infants: theoretical perspectives in 2009. They followed it up the next year with a pilot study demonstrating how to actually administer such therapy. The fact that this approach has been adopted so quickly I think speaks to the principle that this kind of therapy falls into the category of “can’t hurt and might help”. The real question though is does it actually make a difference? Recently, authors from Brazil presented their findings from a single centre double blind RCT entitled Randomized Controlled Trial of Oropharyngeal Colostrum Administration in Very-low-birth-weight Preterm Infants. This authors are commended for studying this practice in such a fashion and included infants <34 weeks who were <1500g at birth to receive the above mentioned intervention. These infants were compared to placebo who received the same intervention except instead of mother’s own colostrum they were given sterile water. In total there were 149 infants randomized with 81 receiving OIT vs 68 who received a placebo. The primary outcome of interest on which a power calculation was performed was the incidence of late onset sepsis. Other typical outcomes including NEC, ROP, BPD, IVH and death were also followed. Did they find a difference? Sadly to many of you I am sure they did not as is shown in the table below. Surprisingly the authors also looked at levels of IgA in infants in both arms and also found no difference. There is a big problem with this study however that no doubt will lead to a repeat version at some point. While the authors enrolled the numbers above, the numbers that were analyzed in the table are 34 lower in the OIT arm and only 2 lower in the placebo group. In essence, a large number of mothers after enrollment were not able to provide the colostrum that was needed for the study. The study called for 48 applications over a 48 hour period and a little more than half of the mothers were able to do it. Do not be dismayed then that no difference was found here. There is no need to “throw the baby out with the bathwater” and abandon OIT based on this one study. I think what is needed in the future though is a study that enrolls far more than needed to account for attrition due to loss of mothers who can complete the study. Without another study I think the practice will continue but does it really make a difference to rates of sepsis? Who knows but there is no doubt it helps parents who are feeling that they have lost control of a pregnancy that has gone wrong, a positive experience and the feeling that they are doing something for their child.
    3 points
  23. Just about all of our preterm infants born at <29 weeks start life out the same in terms of neurological injury. There are of course some infants who may have suffered ischemic injury in utero or an IVH but most are born with their story yet to be told. I think intuitively we have known for some time that the way we resuscitate matters. Establishing an FRC by inflating the lungs of these infants after delivery is a must but as the saying goes the devil is in the details. The Edmonton group led by Dr. Schmolzer has had several papers examined in these blogs and on this occasion I am reviewing an important paper that really is a follow-up study to a previous one looking at the impact of high tidal volume delivery after birth. I have written on this previous paper before in It's possibile! Resuscitation with volume ventilation after delivery. On this occasion the authors have published the following paper; Impact of delivered tidal volume on the occurrence of intraventricular haemorrhage in preterm infants during positive pressure ventilation in the delivery room.This observational study had a simple enough premise. Will the use of Vt > 6 mL/kg in infants given PPV for at least two minutes lead to worse rates of IVH? All infants were < 29 weeks and if they had chest compressions or epinephrine were excluded. All infants were treated equally in terms of delayed cord clamping and antenatal steroid provision. Ventilation was done with a t-piece resuscitator and Vt measured with an NM3 monitor connected to the face mask. First ultrasounds were done for all at 3 days of age. What did the authors find? One hundred and sixty five infants comprised this cohort. Overall, 124 (75%) infants were in the high volume group compared to 41 (25%) with a mean VT<6 mL/kg. Median Vt were 5.3 (4.6-5.7) ml/kg for the low group and 8.7(7.3-10.6) mL/kg which were significantly different. When looking at the rates of IVH and the severity of those affected the results are striking as shown in the table. Hydrocephalus, following IVH developed in 7/49 (14%) and 2/16 (13%) in the >6 mL/kg and <6 mL/kg VT groups. Looking at other factors that could affect the outcome of interest the authors noted the following physiologic findings. Oxygen saturations were lower in the low volume group at 6, 13 and 14 min after birth while tissue oxygenation as measured by NIRS was similarly lower at 7,8 and 25 min after birth (P<0.001). Conversely, heart rate was significantly lower in the VT>6 mL/kg group at 5, 20 and 25 min after birth (P<0.001). Fraction of inspired oxygen was similar in both groups within the first 30 min. Systolic, diastolic and mean blood pressure was similar between the groups. What these results say to me is that despite having lower oxygen saturations and cerebral oxygen saturation at various time points in the first 25 minutes of life the infants seem to be better off given that HR was lower in those given higher volumes despite similar FiO2. Rates of volume support after admission were slightly higher in the high volume group but inotrope usage appears to be not significantly different. Prophylactic indomethacin was used equally in the two cohorts. Thoughts for the future Once a preterm infant is admitted to the NICU we start volume targeted ventilation from the start. In the delivery room we may think that we do the same by putting such infants on a volume guarantee mode after intubation but the period prior to that is generally done with a bag and mask. Whether you use a t-piece resuscitator or an anesthesia bag or even a self inflating bag, you are using a pressure and hoping not to overdistend the alveoli. What I think this study demonstrates similar to the previous work by this group is that there is another way. If we are so concerned about volutrauma in the NICU then why should we feel any differently about the first few minutes of life. Impairment of venous return from the head is likely to account for a higher risk of IVH and while a larger study may be wished for, the results here are fairly dramatic. Turning the question around, one could ask if there is harm in using a volume targeted strategy in the delivery room? I think we would be hard pressed to say that keeping the volumes under 6 mL/kg is a bad idea. The challenge as I see it now is whether we rig up devices to accomplish this or do the large medical equipment providers develop an all in one system to accomplish this? I think the time has come to do so and will be first in line to try it out if there is a possibility to do a trial.
    3 points
  24. While at the #99nicuMeetup, I and @Francesco Cardona were filmed by Miris (one of our exhibiting partners). It was a one-time shot without rehearsal, so we spoke from the heart
    3 points
  25. Recent statements by the American Academy of Pediatric’s, NICHD, the American College of Obstetricians and Gynecologists (ACOG), the Society for Maternal-Fetal Medicine (SMFM), and recommend selective approaches to mothers presenting between 22 0/7 to 22 6/7 weeks. The decision to provide antenatal steroids is only recommended if delivery is expected after 23 weeks. Furthermore the decision to resuscitate is based on an examination of a number of factors including a shared decision with the family. In practice this leads to those centres believing this is mostly futile generally not resuscitating or offering steroids while other more optimistic hospitals having higher rates of proactive (steroids and resuscitation) rates. Then there are other centres where the standard approach is proactive such as one in Uppsala, Sweden where this approach is used almost exclusively. What would happen then if one compared the outcome for infants born at 22 weeks between this hospital and another where a selective approach is generally offered. In this case you would have a lot of experience with resuscitating infants at 22 weeks and the other a fraction of all presenting as a few to many would receive compassionate care. This is exactly what has now happened. A Tale of Two Cities The University Children’s Hospital, Uppsala, Sweden has been compared retrospectively to Nationwide Children’s Hospital, Columbus, Ohio, USA (NCH) with respect to survival and outcomes for their infants born at 22 weeks. The paper by Backes CH et al entitled Outcomes following a comprehensive versus a selective approach for infants born at 22 weeks of gestation tells a very interesting story about the power of belief or faith that one can accomplish something if they set their mind to it. The authors examined a period from 2006-2015, dividing this time into two epochs with the first being 2006-2010 to account for differing practices and resources over time. Given that Uppsala took a proactive approach to all of their 40 live born infants during this time, it provided an opportunity to look at the 72 infants who were live born in the Ohio and examine their differences. In Ohio the approach was as follows; 16 (22%) received proactive care, 18 (25%) received inconsistent care (steroids but no resuscitation), and 38 (53%) received comfort care. In other words, although the total number of infants live born in Ohio was almost double that of Uppsala, only 16 were proactively treated in Ohio compared to all 40 in Uppsala. The differences in outcome are striking Survival in delivery room: (38/40, 95% vs 12/16, 75%; P = 0.049) Provision of delivery room surfactant: (40/40, 100% vs 9/16, 56%; P<0.01) Survival at 24 h (37/40, 93% vs. 9/16, 56%; P < 0.01). Survival to 1 year (21/40, 53% vs. 3/16, 19%; P < 0.05). Among the infants treated proactively, median age of death (17 postnatal days at range 0 h–226 days vs. 3 postnatal hours at NCH, range 0 h–10 days; P < 0.01). All surviving infants had BPD All infants surviving to initial hospital discharge were alive at 18 months’ postnatal age. With respect to long term outcome the authors note: “Outpatient follow-up (qualitative or non-qualitative neurodevelopmental testing) was available in 26 out of 27 infants (96%) Eleven of the 26 (42%) were unimpaired, and all unimpaired infants were in the UUCH cohort. Among the 15 infants with impairment at UUCH, 3 had mild impairment and 12 had moderate or severe impairment. All surviving infants at NCH had moderate or severe impairment.” A word about antenatal steroids as well. In Uppsala 85% of mothers received 2 doses of antenatal steroids vs 25% in Ohio. People sometimes question whether ANS at this age are effective. It is interesting to note that 44% of babies in the Ohio group vs 3% p<0.01 received chest compressions +/- epinephrine in the delivery room. Might this explain the better state of some of these infants at birth? The Power of Belief When I do rounds I often remark that try as we might we can’t will babies to do better. I also commonly say however that we need to be optimistic and although I am accused of seeing the world through rose coloured glasses I think there is an important lesson to be learned from this study. This comparison is really a contrast between a system that believes they can do a good thing for these families by actively promoting a proactive approach vs a system in which I imagine a reluctant approach exists even for those infants where a proactive plan is enacted. One sign of this might be that in Sweden 100% of these deliveries had a Neonatologist present vs 75% in the US. It could be due to other factors such as ability of the Neo to get in within time of the delivery however rather than a sign they didn’t feel they were needed due to futility. There is evidence as well that the aggressiveness of the proactive approach also differs between the two sites based on a couple observations. The first is the rate of surfactant provision in the delivery room which was 100% in Sweden but only 56% in the US. The other thing of note is the time of death for those who did not survive. The median time of death in the US was 3 hours vs 17 days in Uppsala. What does this tell us about the approaches? I would imagine (although the numbers are small) that the teams in the US were much more likely to lose hope (or faith) and withdraw early while the other centre possibility motivated by their past successes pushed forward. Remarkably, although one might think that the teams in Uppsala were simply creating significantly impaired survivors, 42% of the survivors were unimpaired from a developmental standpoint in follow-up. All surviving infants though from Ohio had moderate to severe impairment. What this story may also really be about is practice. The reality is that the team in Sweden had over twice the exposure to such infants over time. Although the number presenting at this GA was higher, the ones that actually were resuscitated and given steroids was less than half. One cannot take away though that Uppsala in the end demonstrated that a proactive approach is definitely not futile. Not only can these children survive but almost half will be developmentally intact. We must acknowledge as well though that since this is a retrospective study there may be factors that may have affected the results. As the saying goes “Individual results may vary”. Are the teams the same in both centres in terms of number of Neonatologists? Are there more residents caring for these infants vs fellows? Are the resources the same? What about proximity of the Neonatologist to the hospital? There are other factors such as cohesiveness of the team and communication between team members that may be influencing the results. In the end though, this is a story of a team that believed it could and did. Perhaps seeing the world through rose coloured glasses is not such a bad thing in the end.
    3 points
  26. One of the first things a student of any discipline caring for newborns is how to calculate the apgar score at birth. Over 60 years ago Virginia Apgar created this score as a means of giving care providers a consistent snapshot of what an infant was like in the first minute then fifth and if needed 10, 15 and so on if resuscitation was ongoing. For sure it has served a useful purpose as an apgar score of 0 and 0 gives one cause for real worry. What about a baby with an apgar of 3 and 7 or 4 and 8? There are certainly infants who have done very well who initially had low apgar scores and conversely those who had higher apgar scores who have had very significant deleterious outcomes including death. I don’t mean to suggest that the apgar scores don’t provide any useful predictive value as they are used as part of the criteria to determine if a baby merits whole body cooling or not. The question is though after 60+ years, has another score been created to provide similar information but enhance the predictive value derived from a score? The Neonatal Resuscitation and Adaptation Score (NRAS) Back in 2015 Jurdi et al published Evaluation of a Comprehensive Delivery Room Neonatal Resuscitation and Adaptation Score (NRAS) Compared to the Apgar Score. This new score added into a ten point score resuscitative actions taken at the 1 and 5 minute time points to create a more functional score that included interventions. The other thing this new score addressed was more recent data that indicated a blue baby at birth is normal (which is why we have eliminated asking the question “is the baby pink?” in NRP. Knowing that, the colour of the baby in the apgar score may not really be that relevant. Take for example a baby with an apgar score of 3 at one minute who could have a HR over 100 and be limp, blue and with shallow breathing. Such a baby might get a few positive pressure breaths and then within 10 seconds be breathing quite well and crying. Conversely, they might be getting ongoing PPV for several minutes and need oxygen. Were they also getting chest compressions? If I only told you the apgar score you wouldn’t have much to go on. Now look at the NRAS and compare the information gathered using two cardiovascular (C1&2), one neurological test (N1) and two respiratory assessments (R1&2). The authors in this study performed a pilot study on only on 17 patients really as a proof of concept that the score could be taught and implemented. Providers reported both scores and found “superior interrater reliability (P < .001) and respiratory component reliability (P < .001) for all gestational ages compared to the Apgar score.” A Bigger Study Was Needed The same group in 2018 this time led by Witcher published Neonatal Resuscitation and Adaptation Score vs Apgar: newborn assessment and predictive ability. The primary outcome was the ability of a low score to predict mortality with a study design that was a non-inferiority trial. All attended deliveries were meant to have both scores done but due to limited numbers of trained personnel who could appropriately administer both scores just under 90% of the total deliveries were assigned scores for comparison. The authors sought to recruit 450 infants to show that a low NRAS score (0–3) would not be inferior to a similar Apgar at predicting death. Interestingly an interim analysis found the NRAS to be superior to Apgar when 75.5% of the 450 were enrolled, so the study was stopped. What led the apgar score to perform poorly in predicting mortality (there were only 12 deaths though in the cohort) was the fact that 49 patients with a 1 minute apgar score of 0-3 survived compared to only 7 infants with a low NRAS score. The other interesting finding was the ability of the NRAS to predict the need for respiratory support at 48 hours with a one minute apgar score of 0-3 being found in 39% of those on support compared to 100% of those with a low NRAS. Also at 5 minutes a score of 4-6 for the apgar was found in 48% of those with respiratory support at 48 hours vs 87% of those with a similar range NRAS. These findings were statistically significant while a host of other conditions such as sepsis, hypoglycemia, hypothermia and others were no different in terms of predictive ability of the scores. An Even Bigger Study is Needed To be sure, this study is still small and missed just over 90% of all deliveries so it is possible there is some bias that is not being detected here. I do think there is something here though which a bigger study that has an army of people equipped to provide the scoring will add to this ongoing story. Every practitioner who resuscitates an infant is asked at some point in those first minutes to hour “will my baby be ok?”. The truth is that the apgar score has never lived up to the hope that it would help us provide an accurate clairvoyant picture of what lies ahead for an infant. Where this score gives me hope is that a score which would at the very least help me predict whether an infant would likely still be needing respiratory support in 48 hours provides the basic answer to the most common question we get in the unit once admitted; “when can I take my baby home”. Using this score I could respond with some greater confidence in saying “I think your infant will be on support for at least 48 hours”. The bigger question though which thankfully we don’t have to address too often for the sickest babies at birth is “will my baby survive?”. If a larger study demonstrates this score to provide a greater degree of accuracy then the “Tipping Point” might just be that to switching over to the NRAS and leaving the apgar score behind. That will never happen overnight but medicine is always evolving and with time you the reader may find yourself becoming very familiar with this score!
    3 points
  27. July was very eventful for me and that had caused my on-line silence. I had a chance to visit again my beloved Finland and now I'm back with fresh thoughts and ideas (and also hundreds of photos). Enjoy! Kotiloma is a word in Finnish that means „vacation at home”. But in some NICUs around Finland it has grown into a bit different meaning. Kotiloma is a practice of arranging a little vacation at home for NICU patients before their final discharge. The routine is quite simple. On the kotiloma day parents come to the unit with a car seat and a set of clothes. When the seat is warm and the baby is ready, they just simply take their baby home for a day. Before they leave, they inform the staff about the time of their return. If they would feel insecure, they can always return to the unit sooner and their room will be waiting for them. The duration of the stay away from the unit can last from a couple of hours up to a whole weekend. Sounds interesting? There are two basic conditions: parents' willingness and staff's trust in parents' abilities. Parents need to be confident when it comes to securing baby’s needs. Since kotiloma applies mostly to preemies, parents are generally well prepared (hello Family Centered Care!) and very eager to take the baby home for this vacation. It’s like a free trial of full-time parenthood and you can still bring the baby back But seriously speaking, after spending several weeks in the unit with the baby, they really just want to change the surroundings and go out for a while. If the home is too far away, or if the thing is just logistically too difficult, they can take their child for a long walk in a baby stroller instead. Since parents are in the unit every day, taking care of their little one, it is quite simple for the medical staff (especially for the fantastic nurses!) to assess their preparedness, encourage them and prepare them also technically for kotiloma. Basically there are two types of kids who go for a vacation to home. The first one is when the baby is being fed by a feeding tube and getting close to the discharge date. Parents generally feel quite comfortable with using the tube and since they are practically living in the unit, it’s not a big hassle for them to take the baby home with this tube. The second group of babies are the ones on an "apnea countdown" . Those are sent home with saturation monitors and parents are specifically educated by nurses to interpret heart rate and SatO2. They are additionally trained in infant resuscitation. This whole „crash course” takes no more than 1 hour. If the parents are eager for the kotiloma and the staff is ready to train them, they can take the baby home for the daytime (so they can observe the monitors, but those babies have to return to the Unit for the nighttime.) If you are even a bit like me, and I know many of you are, you will ask „BUT WHO IS LEGALLY RESPONSIBLE FOR THAT BABY? WHO IS IN CHARGE IF ANYTHING HAPPENS?”. Well, since the kid is not really discharged from the hospital, that would be you. I know it sounds tricky, but my (not-so-)confidential informant Samuli Rautava from the TYKS NICU says, that since they’ve been doing that (already 5 years!), nothing has ever happened. If the family has any questions or concerns during the kotiloma, they are encouraged to call the nursing station. They are never left alone with their worries. When it comes to financial issues, I would say (naively) that nobody pays anything extra for that vacation. Since the kid hasn’t been discharged, the healthcare fund pays for the day in the unit. Parents provide their own car, clothes and the car seat. No more costs are involved. Easy as that Is it safe? Generally life is known to be a dangerous adventure But it’s easy to notice, that this practice is based on a mutual trust agreement. "You- The Parents- trust us- The Medical Staff- every day, that we perform medical procedures based on our best knowledge and best available evidence. So WE trust YOU, that you will not idle away our efforts and do your best to provide the best possible care to your baby". This cooperation is working well. Parents are properly educated in their baby’s needs (thanks to Close Collaboration with Parents Training Program). They learn how to perform CPR and call 112 in case of emergency. The nursing staff always gets the information about the condition of other siblings and cohabitants (to avoid infections etc). Okay, but what are the benefits? Besides empowerment of the parents (which is a huge thing, especially since they are on-their-way to the discharge date), it actually makes the whole discharge process easier. After the kotiloma parents' confidence grows. It is like a short trial of full stay-at-home parenthood. When you take your precious, fragile baby home, some questions may arise in your head. It feels good to know, that you will be able to ask them to your own pediatrician and nurses when you return to the unit. This practice enables parents to observe their child in a home setting. They notice how the baby looks around and curiously contemplates the new environment. It is also a good chance for other cohabitants (those furry ones too!) to get to know their future housemate. Kotiloma is simply a joy for parents, baby and whole family. A sign saying „our baby is doing fine”. Some happy moment to cherish. We all need those sometimes!
    3 points
  28. I had an amazing opportunity to visit NICU in the Turku University Hospital in 2016. They admit around 550 problematic newborns per year. About 10% of them are born below 30 weeks of gestation. The whole unit is practically based on 11 family rooms (single family rooms when possible) and additionally one larger room for 4 patients. The larger room is usually used for babies who are admitted due to transient issues (tachypnea, hypoglycemia, hyperbilirubinemia etc). Single family rooms are equipped with an incubator/open warmer bed/cot, one adult bed, one reclining armchair and a nappy changing station. There is also a breast pump and a refrigerator for breast milk in the room. Parents are constantly involved in the care of their preterm baby and are welcome to stay and care for their child all day and night. That’s the theory. So what is the reality? Entering the unit for the first time, the word that came to my mind was „serenity”. The unit welcomes you with knitted octopuses and tiny socks everywhere. The whole design of the unit is somehow soft, warm and calming. Each family room is „protected” by a closed door with a window in them - and the window is also covered with a pastel-color quilt. If you want to enter the room, or you’re just looking for your co-worker, you can just „peek in” and check without disturbing the family much. Then you can knock on the door and enter the room. This way you are giving the family the maximum privacy we can offer in those special circumstances. Well, you have those tiny, „problematic” children in those private family rooms, with their parents being their primary caretakers, guardians and gate-keepers. Yet, nobody feels that their access to the patient is limited. How is that even possible? Maybe this is what we call „the change of the caring culture”? When you’re „letting go” of some of your duties and delegating them to the parents, you also learn to trust them with your little patient. After all, we all have the same goal- and the parents are personally and emotionally interested in their own child’s well-being, so they have even stronger motivation to perform well. Visiting you patient in the single family room feels like visiting your friends, who had just brought their newborn back from the hospital. Imagine the situation, that you’re paying them that first visit, with a little gift wrapped in a pink paper and a big pink balloon. What will you expect? I think it’s quite normal that their room will be a bit messy and everybody will be whispering around the sleeping baby. It’s normal that the mother will be breastfeeding (or pumping milk) in your presence. And again- it’s normal that parents will be touching and cuddling the baby. I’ve visited several neonatal intensive care units around the Europe. They all announce proudly, that they are „family centered units”. They all know that skin-to-skin care is a recommended, good and beneficial procedure. Yet in the same time, they actually treat it like a medical procedure - which is time-limited and full of exclusion criteria. That procedure also seems to be quite stressful for the medical staff, because they feel like they can’t access their patient anymore. What if something happens, what if we need to react, how to save that baby when the baby is outside the cot? How can we be medical professionals, when the patient is out of reach? It comes straight to the question: what exactly is skin-to-skin care for you? Is it a medical procedure, which is performed once or twice a week, for one hour, when the baby (and the parent!) is fully dressed? Or do you consider mother’s and father’s bare chest as a new space of care for your patient? A safe surrounding, stabilizing baby’s body temperature, breathing and heart rate? And what do you consider a contraindication for skin-to-skin care? Recently I’ve heard from my friend that in their NICU (highest reference centre) kangaroo care is performed only after the baby reaches 1600g. In other place, I’ve seen a healthy 31-weeker in his second week of life, on full enteral feeds, happily kicking in a closed incubator, who couldn’t be kangarooed or even touched by his parents, just because there was a PICC-line placed in his arm. I still remember those sad parents, wearing plastic gowns, standing by that closed incubator, not being able to even touch their own baby, just because it was a preemie. Prematurity is a diagnosis, but it’s not a sentence! If we are treating similar babies with similar equipment and similarly trained staff - why does our practice differ so much? Leave your comment and join the discussion!
    3 points
  29. I met the author of this article at a CPS meeting a few years ago, she immediately impressed me with her unique perspective. Paige is a developmental pediatrician who does long-term follow-up of preterms, and is involved in developmental evaluation and intervention of children with other challenges, including Spina Bifida. Church P. A personal perspective on disability: Between the words. JAMA Pediatrics. 2017. As you will see if you read the article, Paige has a form of Spina Bifida herself, a Lipomyelomeningocele, with a neurogenic bladder and neurogenic bowel, requiring life-long interventions. She discusses the poor tolerance many medical people have of disability, and such how things are often discussed as black or white, whereas having a profound personal experience of disability has made her much more nuanced. She recounts being involved in a discussion regarding a "selective reduction" of a twin pregnancy where the twin being considered for "reduction", i.e. abortion, had a similar lesion to her own. That is an experience that I can barely understand: how would I react if a family was considering terminating a pregnancy because of a condition that I had? Paige recounts the episode with tact and humanity. I can imagine, as I have heard them many times, the words of the other physicians involved in such a decision, I am sure they talked about handicaps and limitations, poor quality of life, pain, and restrictions on family life. Most of which is said with good intentions but with no real knowledge of the literature, or of the range of experiences of families living with the challenges. Just as with similar discussions regarding extreme preterm infants, a list of complications, interventions, disabilities, and long-term problems is often presented, but with no similar list of benefits, achievements, abilities, long-term adaptation, and happiness. Near the end of her moving piece Paige writes: Like most things in life, and medicine, disability is sharp, painful, humbling, as well as tremendous, giving, awe-inspiring. It is human. It is not easily distilled to an all or none discussion. Medicine sets the tone for this discussion and, to date, has done a miserable job. More is needed to appreciate the incredible opportunities that disability poses. More education is needed to provide the counselling families deserve: balanced, sensitive, thoughtful, and individualized rather than “objective.” I sincerely hope that this piece by Paige will be part of a new discussion about these issues. (Of note, even though the article is behind a paywall, JAMA lets you see the first page of the article before buying, in this case there is only one page, so you can read the whole thing for free!)
    3 points
  30. 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?”
    3 points
  31. This may sound familiar as I wrote about this topic in the last year but the previous post was restricted to infants who were under 1000g. High Flow Nasal Cannula be careful out there had a main message that suggested the combined outcome of BPD or death was more prevalent when HFNC is used alone or with CPAP than when CPAP is used alone. The question remains though whether this applies to larger infants. Without looking at the evidence for that combined outcome most people would say there is unlikely to be a difference. Larger more mature babies have a much lower risk of BPD or death so proponents of HFNC would say it is simpler to use and helps prevent nasal breakdown as well. The question remains as to whether all outcomes are the same in larger infants and that is the point of this post. A Non-Inferiority Trial First off it is important to understand what this type of trial is. The first requirement is that the two treatments have both been compared to a placebo and found to be both effective. Once you establish that you have a choice between two treatment options then you eliminate the placebo and compare them head to head. What you are looking for in this type of trial is to determine not whether one is better than the other but that there is no difference in a clinical outcome of interest. If you find no difference then the next step is to look at other outcomes that might be of interest and see if there are any benefits to picking one versus the other. In the case of CPAP vs HNFC, if a non-inferiority trial showed no difference in an important outcome such as length of stay but nasal breakdown was less with HFNC it might lead a unit to use HFNC for their infants. Okay, now that we have that cleared up we can move on to an actual study examining this very subject. Nasal High-Flow Therapy for Primary Respiratory Support in Preterm Infants. This was an interesting study with a great name (The HIPSTER trial) that enrolled infants > 28 weeks and 0 days with none of the infants receiving surfactant but either being randomized to HFNC or CPAP after delivery. These infants were your typical modern day cohort of babies who may avoid intubation and surfactant by establishing FRC early with positive pressure applied to the nose through one of these devices. The end point for the study was treatment failure within 72 hours. If an infant failed in the HFNC they could have a trial of CPAP whereas in the CPAP group they were intubated. For each infant in the HFNC group flow was set from 6-8 l/min and for CPAP 6-8 cmH2O. Treatment was considered to have failed if an infant receiving maximal support (high-flow therapy at a gas flow of 8 liters per minute or CPAP at a pressure of 8 cm of water) met one or more of the following criteria: FiO2 of 0.4 or higher Arterial or free flowing cap gas with a pH of 7.2 or less plus a pCO2 > 60 mm Hg obtained at least 1 hour after starting treatment Two or more episodes of apnea requiring positive-pressure ventilation within a 24-hour period or six or more episodes requiring any intervention within a 6-hour period. Infants with an urgent need for intubation and mechanical ventilation. So what happened? The trial randomized 583 infants (278 HFNC, 286 CPAP) but was halted by the data and safety monitoring committee after an analysis of the first 515 revealed that the outcome was worse in the HFNC group (25.5% failure rate vs 13.3 for CPAP). Interestingly treatment failures were more common in babies below and above 32 weeks so it was not just the smallest infants who failed. Another interesting finding was that the most common reason for treatment failure was criteria 1 (FiO2 > 40%) while intubation was higher for all infants but did not reach statistical significance. Curiously what did reach a significant difference was criteria #4 (18.4% urgent intubations in the CPAP group vs 5.6% in the HFNC group). You might be tempted to therefore ponder which is worse, a little O2 or being intubated but you need to recall the trial design which was set up to provide this kind of result. If you failed HFNC you were placed on CPAP whereas if you failed CPAP you were intubated. In the HFNC group, 78 infants were deemed to have failed but 28 of them were in fact “rescued by CPAP”. It therefore isn’t a fair comparison when it comes to urgent intubation since if you failed CPAP there wasn’t another option. Not a total loss Nasal trauma was indeed much lower in the HFNC group, occurring only 8.3% vs 18.5% of the time with CPAP. Pneumothorax was also found to be significantly different with none of the patients in the HFNC group having that complication vs 2.1% in the CPAP group. What this study tells us is that as a primary modality to treat newborns with RDS who have not received surfactant it is preferable to use CPAP in the first 72 hours. Some of you may say it might not say that at all but consider the impact of having more babies exposed to high FiO2. We know from other studies that high FiO2 can be quite damaging to preterm infants and this study was certainly not powered to look at all those important outcomes such as ROP, PVL and BPD. The authors report them and found no difference but without adequate power to show a difference I wouldn’t take much comfort in those findings. I think were things may settle out though is what to do in more mature infants. There is no question that for those on chronic respiratory support there is some risk of nasal breakdown. Although I don’t have much experience with HFNC I would think that for the older patient who either already has BPD at 36 weeks or is close to that point but reliant on +4 or +5 CPAP that HFNC might help “give them a break”. As such I don’t see this as a total loss but rather an option to try when CPAP for whatever reason is not tolerated. As a primary therapy for non-invasive management RDS I will keep my CPAP for all babies thank you.
    3 points
  32. This publication appeared on-line a couple of months ago, and still isn't in print. Prentice T, et al. Moral distress within neonatal and paediatric intensive care units: a systematic review. Arch Dis Child. 2016. It is a systematic review from Melbourne, with the help of Annie Janvier, of the literature surrounding moral distress in health care workers in the NICU and the PICU. All of the studies included nurses, and some of them also studied other health care workers. Moral Distress refers to subjective feelings of distress in response to the ethical challenges of health care work. It is a term which first appeared in the nursing literature, and, although other terms have been suggested, I think it fits. Moral residue is another term these authors refer to, which is the lingering feelings which persist after the "morally distressing" case has ended. As we deal with children and babies who are fragile, dependent, and may have life-long complications, the NICU and PICU are places where moral distress is likely to be frequent. How frequent it is, and what causes the situations most likely to lead to distress, where the questions that lay behind this systematic review. They found 13 articles, of varying size and quality, (including one of ours); from the results of the systematic review article: One of their findings is the different ways in which moral distress is discussed in the articles, publications in the nursing literature frequently emphasize the subjective experience of the nurses, and the fact that they lack power and are having to provide interventions that they do not always agree with; they are sometimes portrayed as the victims of the aggressive care being perpetrated by the physicians. Whereas in the medical literature moral distress is described in terms of the objective situations that create confrontations or dilemmas. The reality is though, that physicians also experience moral distress (with about the same frequency as nurses), they also find themselves sometimes performing tasks and providing care which is against their own conception of what the best interest is for their patients. What has been shown previously is that moral distress may lead to burnout, and decrease retention of staff. It is also probably unavoidable in intensive care, but we should, and could, work harder to minimize it, and minimize its impact.
    3 points
  33. As I was preparing to settle in tonight I received a question from a reader on my Linkedin page in regards to the use of sustained inflation (SI) in our units. We don't use it and I think the reasons behind it might be of interest to others. The concept of SI is that by providing a high opening pressure of 20 - 30 cm H2O for anywhere from 5 to 15 seconds one may be able to open the "stiff" lung of a preterm infant with RDS and establish an adequate functional residual capacity. Once the lung is open, it may be possible in theory to keep it open with ongoing peep at a more traditional level of 5 - 8 cm of H20. The concept was tested 25 years ago by Vyas et al in their article Physiologic responses to prolonged and slow-rise inflation in the resuscitation of the asphyxiated newborn infant. In this study, 9 newborn infants were given a relatively short 5 second sustained inflation and led to earlier and larger lung volumes with good establishment of FRC. Like many trials in Neonatology though sceptics abound and here we are 25 years later still discussing the merits of this approach. As I have a warm place in my heart for the place that started my professional career whenever I come across a paper published by former colleagues I take a closer look. Such is the case with a systematic review on sustained inflation by Schmolzer et al. The inclusion criteria were studies of infants born at <33 weeks. Their article provides a wonderful assessment of the state of the literature on the topic and I would encourage you to have a look at it if you would like a good reference to keep around on the topic. What it comes down to though is that there are really only four randomized human studies using the technique and in truth they are fairly heterogeneous in their design. They vary in the length of time an SI was performed (5 - 20 seconds), the pressures used (20 - 30 cm H2O), single or multiple SIs and lastly amount of oxygen utilized being 21 - 100%. In fact three of the four studies used either 100% or in one case 50% FiO2 when providing such treatments. What Did They Show? This is where things get interesting. SI works in the short term by reducing the likelihood that an infant will need mechanical ventilation at 72 hours with a number needed to treat of only 10! In medicine we normally would embrace such results but sadly the results do not translate into long term benefits as the rate of BPD, mortality and the combined outcome do not remain significant. Interestingly, the incidence of a symptomatic PDA needing treatment with either a medical or surgical approach had a number needed to harm of 11; an equally impressive number but one that gives reason for concern. As the authors speculate, the increased rate of PDA may be in fact related to the good job that the SI does in this early phase. By establishing an open lung and at an earlier time point it may well be that there is an accentuation in the relaxation of the pulmonary vasculature and this leads to a left to right shunt that by being hemodynamically significant helps to stent the ductus open at a time when it might otherwise be tending to close. This outcome in and of itself raises concern in my mind and is the first reason to give me reason to pause before adopting this practice. Any other concerns? Although non-significant there was a trend towards increased rates of IVH in the groups randomized to SI. There is real biologic plausibility here. During an SI the increased positive pressure in the chest could well simulate a similar effect to a pneumothorax and impede the passive drainage of blood from the head into the thorax. In particular, longer durations and/or frequent SIs could increase such risk. Given the heterogeneous nature of these studies it is difficult to know if they all had been similar in providing multiple SIs could we have seen this cross over to significant? I believe the biggest concern in all of this though is that I would have a very hard time applying the results of these studies to our patient population. The systematic review addresses the question about whether SI is better than IPPV as a lung recruitment strategy in the preterm infant with respiratory distress. I have to say though we have moved beyond IPPV as an initial strategy in favour of placement of CPAP on the infant directly after birth. The real question in my mind is whether providing brief periods of SI followed by CPAP of +6 to +8 is better than placement on CPAP alone as a first strategy to establish good lung volumes. If I am to be swayed by the use of SI someone needs to do this study first. The possibility of increasing the number of hemodynamically significant PDAs and potentially worsening IVH without any clear reduction in BPD is definitely placing me firmly in the camp of favouring the CPAP approach. Having said all that, the work by the Edmonton group is important and gives everyone a glimpse into what the current landscape is for research in this field and opens the door for their group or another to answer my questions and any others that may emerge as this strategy will no doubt be discussed for years to come.
    3 points
  34. We live in a world at the moment where the public has become increasingly aware of the dangers of antibiotic overuse. Parents are more than ever requesting no erythromycin for the eyes after birth, and even on occasion questioning the need for antibiotics after delivery for the infant with risk factors for sepsis. The media has latched on to the debate as well by publishing the sensational articles about superbugs and medicine running out of the last lines of defence such as this article from the CBC. As teams caring for newborns both preterm and term we are also increasingly aware of the dangers of altering the microbiome of these vulnerable infants with antibiotic overuse. Some babies robbed of the vaginal microbiome when delivery occurs by C-section, have their parents swabbing their newborn with vaginal secretions to populate their child with the "good bacteria" that come through a "natural" delivery although recent commentary questions the safety of such practice. Infants born through meconium stained amniotic fluid can certainly become sick after delivery. Inhalation of meconium in the sickest infants often occurs during gasping episodes in utero after hypoxic stress causes evacuation of the rectal contents. The fetuses who inhale this material may go on to develop, inflammatory changes, areas of atelectasis and hyperinflation and pulmonary hypertension; the so called meconium aspiration syndrome. These infants of course may be extremely sick and need high frequency ventilation to manage their CO2 retention and in some cases may go on to ECMO although with inhaled nitric oxide this has become less common. As another consideration, could infection such as chorioamnionitis be the inciting event to cause passage of meconium in utero? The health care team though for as long as I have been in practice would add to the treatment plan a course of antibiotics. In fact I would guess that many Neonatologists the world over have uttered the phrase "They are REALLY sick, please start antibiotics". The real question though is whether the baby is in fact infected. Meconium is certainly a good growth medium for bacteria but with the short time from passage to delivery in most cases I doubt there is much time for significant growth. Moreover, I have found myself saying many times that such infants have a chemical pneumonitis and have often questioned whether antibiotics are really needed. Nonetheless it would take nerves of steel in some cases to not use antibiotics in these patients. Then along came this study Role of prophylactic antibiotics in neonates born through meconium-stained amniotic fluid (MSAF)—a randomized controlled trial by Goel A et al. This study was done prospectively by randomizing newborns born through meconium stained amniotic fluid to either antibiotics (N=121) for three days or no antibiotics (N=129) after diagnosis. In each case blood and CRP were drawn and if the infant was symptomatic (presence of respiratory distress, lethargy, abdominal distension, temperature or hemodynamic instability, hypoglycemia, apnea, or any other systemic abnormalities) a lumbar puncture and chest x-ray were added. The primary outcome variable was defined as " the incidence of early (within first 72 h of birth) or late onset (after 72 h of birth) suspect sepsis (clinical symptoms or positive sepsis screen defined as ≥2 positive parameters) and confirmed sepsis (positive blood culture)." Results Clinicians in the study were allowed to continue antibiotics past the 72 hours or start antibiotics in the no antibiotic group if they considered an infant to have suspected sepsis or in fact were found to be proven. The outcomes for those possibilities are shown below. Taking it all together whether you started antibiotics or not the primary outcomes were no different. Furthermore there is no apparent harm based on outcomes that matter including the most important; death (3 in each group) that it does give one reason to pause when considering whether to treat prophylactically with antibiotics for babies born through meconium stained fluid. What About The Sickest of The Sick When attempting to answer this question the authors noted the following. "On doing a subgroup analysis on incidence of sepsis in symptomatic babies (presenting with respiratory distress), both groups were found to have comparable incidence of suspect sepsis (p=0.084). The incidence of confirmed sepsis was more in symptomatic babies, although the total numbers was very few (p=0.01)" Herein lies the challenge in declaring once and for all that we don't need antibiotics at all in MAS. While the study was powered to adequately answer the primary outcome, the subgroups are so small that declaring with any confidence that one can stand by and watch infants with severe MAS without starting antibiotics is a tough conclusion to come to. The child though who is born through MSAF and has mild tachypnea as the only symptom I suspect is another story. I might even argue that the baby who is in need of CPAP could be watched and if they deteriorate have antibiotics started. As much as I would love to say none of these babies need antibiotics I would have to admit that I would cave once the baby was ventilated. It is better to provide a couple of days of antibiotics while awaiting blood cultures than to have a patient with sepsis left untreated or at least that is my opinion. The question is what would you do?
    3 points
  35. I don't know about you but I have deeply rooted memories from the 1990s of donning a yellow gown and gloves before examining each and every patient on my list before rounds. This was done as we firmly believed such precautions were needed to prevent the spread of infections in the NICU. As time went on though the gowns were removed and not long after so went the gloves as priority was placed on performance of good hand hygiene to reduce rates of infection in our units. You can imagine that after having it entrenched in my mind that hand hygiene was the key to success that I would find it surprising to see a paper published a few months ago suggesting that the use of gloves after hand hygiene may offer a benefit after all. Kaufman DA et al published Nonsterile glove use in addition to hand hygiene to prevent late-onset infection in preterm infants: randomized clinical trial and given it's challenge to a practice that is at least two decades old I thought it may be worth sharing with you the reader. Essentially the authors hypothesized that the use of non-sterile gloves after performing hand hygiene (compared to hand hygiene alone) would reduce late-onset invasive infection (>72 hours after birth), defined as 1 or more episodes per patient of a BSI, urinary tract infection,meningitis, and/orNEC associated with clinical signs and symptoms of infection and treated with antimicrobials. When determining the size of study needed, they used a baseline incidence of 60% and looked to find a 25% reduction in their outcome. Unfortunately for them (although very fortunate for their patients, the incidence of LOS in the experimental arm was 32% with a 45% incidence in the control group (hand hygiene alone). What does this mean when your expected rate is higher than your observed? In short you need more patients to show a difference and indeed they failed to show a significant difference between the two groups. They did however find a difference in gram positive infections being 15 vs 32% p=0.03 and seem to take some comfort in this finding. If you were to give the paper a quick read you might be impressed with the finding and might even shrug your shoulders and say the common expression "Can't hurt but might help" Maybe we should adopt this? Not so Fast There is a significant potential source of error here that needs to be addressed. The definition of a proven blood stream infection as per the CDC is two positive cultures for the same organism. In this study only one culture was required to be positive so the potential for diagnostic error is high. In our own centre although unpublished we have noted since adopting a mandatory two culture collection approach for LOS that there have been a significant number of occasions where one culture was noted to be positive and the other negative. Antibiotics in these cases have been stopped (for gram positive organisms) after 48 hours without consequence. In this study however the findings of increased rates of positive cultures in the hand hygiene only group is heavily influenced by the presence of only one positive culture as is seen in this table. When looking at the numbers of times there were greater than or equal to 2 positive cultures in the CoNS group one sees the vast majority were only based on one culture. Furthermore, of the 20 infections in the hand hygiene only group, 19 were gram positve CoNS of which only 4 had more than one culture. Based on this finding and the lack of any other significant difference in infectious outcomes the proof that gloves add anything to reducing infection rates is tough to argue. Could Gloves Actually Make Things Worse? Several studies have actually indicated that wearing gloves reduces hand hygiene compliance. One such study although in adults "The dirty hand in the latex glove": a study of hand hygiene compliance when gloves are worn. suggests that this is indeed the case with a 9% decrease in proper hand hygiene when gloves were worn. Others such as Flores in 2006 found similar poor perfomance when gloves were used Healthcare workers' compliance with glove use and the effect of glove use on hand hygiene. I would speculate that although we all want to do what is best for our patients there may be a psychological trick being played here. Perhaps knowing we will cover up with gloves leads people to take shortcuts on hand hygiene as they subconciously think they will be covered anyway. Never mind that the "dirty" hand touches the gloves they will put on making proper hand hygiene a must. Conclusion It certainly was a shock to see such a paper as I saw flashes of my past yellow gowned self coming back to haunt me. Based on my take of this paper however I would say that at least for the time being I will take my time, wash my hands before and after every patient encounter and keep the gloves around for handling those yet unbathed newborns. Spend your energy where it counts and that is ensuring your hands are properly cleaned before touching your patient or lines.
    3 points
  36. I have often wondered why my obstetrical colleagues would often induce labour once a woman with ruptured membranes reached 34 weeks. I wasn't aware of any data to support doing this, or, on the other hand, any good data to say that you shouldn't. It turns out that I was well-informed, there just wasn't any good data, until now. Morris JM, et al. Immediate delivery compared with expectant management after preterm pre-labour rupture of the membranes close to term (PPROMT trial): a randomised controlled trial. Lancet. 2015;387(10017):444-52. In this study over 1800 women with singleton pregnancies and ruptured membranes without labour, who were between 34 and 37 weeks gestation, were randomized to either immediate delivery (induction or cesarean) or expectant management, in which case the woman and her obstetrician waited for spontaneous labour or another indication to deliver. Women whose membranes ruptured before 34 weeks became eligible when they hit that mark. This remarkable study took 10 years to recruit their subjects. It was run out of Sydney, and funded by the NHMRC of Australia and enrolled mothers from 11 different countries. What did they find? Well, neonatal sepsis occurred in 23 (2%) of the babies in the immediate delivery group, 29 (3%) of the expectant group, a difference which could easily be due to chance. There were 3 neonatal deaths in each group. On the other hand, expectantly managed pregnancies ended up with a significantly higher gestational age and birthweight, not surprisingly, and as a result less NICU admission, less respiratory distress, less assisted ventilation, and fewer days in hospital, all of which were highly statistically significant. For the mothers there were some downsides, there was a slight increase in antepartum or intrapartum haemorrhage from 3% to 5% and they had one day more of hospital stay with expectant management, but they had many fewer cesarean deliveries. 19% in the expectant group compared to 26%. This is very high quality evidence that we should not be doing what ACOG currently states, which is to deliver immediately because of the risk of neonatal sepsis. If things are going well, and there is no sign of infection, pre-labour preterm rupture of membranes can be followed closely, with delivery for other obstetric indications.
    3 points
  37. Many of you will have heard of the "Choosing wisely" campaign, an attempt to improve decision making, by clarifying efficacy and risks of common procedures or therapies. Many specialty societies have come up with lists of the Top-5 questionable practices that should be reconsidered. The AAP has just published a list of 5 neonatal practices that they say should be avoided. It is interesting that some of the other societies have made very clear recommendations to not do certain things (“Don’t do….” a particular test, for example). The AAP list instead states to “Avoid Routine…” for each one of the 5 practices. I think for a couple of their practices they could have been more forthright. 1. Avoid routine use of antireflux medications for treatment of symptomatic GERD or for treatment of apnea and desaturation in preterm infants. This is one where that prior comment applies. I think this should have been stated “Do not use antireflux medications in the newborn”. The reason being that there is no such animal. There is no medication that has been shown to reduce reflux. There is no way clinically to diagnose abnormal reflux. There is no effect of antireflux medication on apnea or desaturation. All the medications in use are toxic. Now if by antireflux medications, they include anti-gastric acidity medications (and when you look at the supplemental materials it seems that they do) then I guess you could temper those comments a little. It is possible that sometimes acid-caused reflux disease is an issue, and the agents are effective at reducing gastric acid production, even in the newborn. Whether they improve any acid-related disease findings is less certain, most of the rare small RCTs have shown no clinical benefit. They are also associated with more infections, more NEC and increased mortality in the preterm. So maybe in a baby after diaphragmatic hernia repair, or after Oesphageal Atresia repair they could be indicated, but it would be great to have some actual data. 2. Avoid routine continuation of antibiotic therapy beyond 48 hours for initially asymptomatic infants without evidence of bacterial infection. Again I think this could be a stronger statement, given the 2 provisos that the babies are initially asymptomatic and that they have no evidence of bacterial infection. In other words it is for babies with risk factors for infection, but who develop no clinical signs. In those babies you could appropriately say “Stop antibiotics at 36 hours”. 3. Avoid routine use of pneumograms for predischarge assessment of ongoing and/or prolonged apnea of prematurity. I think this is appropriately stated, there may be indications for selective predischarge pneumograms, for diagnostic rather than screening purposes, so “Avoid routine” is about right. 4. Avoid routine daily chest radiographs without an indication for intubated infants. I agree with this, I didn’t know it was a common practice in the NICU. Some babies are intubated for months, that would be an awful lot of radiation. 5. Avoid routine screening term-equivalent or discharge brain MRIs in preterm infants. Again I agree with this, as many of you will already know! The justification given however, is that there is no evidence that they improve long term outcome. While that is true, I don’t think that is why they are being done, not many people think a few minutes in a magnet will make the babies better. The data show a poor positive predictive value of abnormal findings for long term outcomes, which make them of questionable value.
    3 points
  38. All food is brain food when your brain is making 250,000 new neurones every minute. In a small two-center trial first published in 2013 50 very preterm babies were randomized to different parenteral nutritional intakes. The main differences between the groups were that the controls started at 2 g/kg/d of protein, compared to 3.5 in the intervention group. The controls started at 0.5 g/kg/d of lipid given as ClinOleic, the intervention group started at 2 of SMOFLipid; both gradually increased to a max of 3.4. One they were receiving 110 mL/kg/d of milk the fortification was different between the groups, with the enhanced group getting an extra 0.8 g/kg/d of protein, to achieve 4.4 g/kg/d, and getting extra omega 3 fatty acids to arrive at a total of 166 kcal/kg/d, compared to 146. (which is a whole lot of calories!) Unfortunately the planned sample size was not achieved, the study was stopped early because there was more sepsis in the enhanced nutrition group (p<0.04). Stopping a trial for a barely significant difference between groups is really not a good idea, but it is often a difficult decision, especially when the difference is an important adverse outcome. The primary outcome was post-natal growth restriction. The authors were following a number of secondary outcomes as were the data monitoring committee. The risk that one of those outcomes will be 'statistically significant' at some point during the data accumulation is enormous. That is why stopping rules should be much more stringent than that. Of course if you continue the study and it turns out that there really is more sepsis at the end of the study, you may then be criticized, and you might feel bad. You might indeed face totally ridiculous criticisms similar to those that were directed at the SUPPORT trial by Public Citizen, who don't understand how interim analyses work. Having said that the authors published a second paper with the growth data; because of the small sample size there was a difference in the birth growth variables between groups, which actually favoured the controls, more SGA babies in the enhanced nutrition group. Despite this there were significant advantages of the enhanced protocol. None of the non-growth restricted babies in the intervention group became growth restricted, compared to 1/3 of the babies in the control group. The z-scores for weight dropped by about 0.3 for the intervention group, between birth and 30 days of age, and by about 0.7 in the controls. Head growth was also better. A subset of the infants had MRI performed at term, which has just been published, and which is why I am writing this post. Strømmen K, Blakstad EW, Moltu SJ, Almaas AN, Westerberg AC, Amlien IK, et al. Enhanced Nutrient Supply to Very Low Birth Weight Infants is Associated with Improved White Matter Maturation and Head Growth. Neonatology. 2015;107(1):68-75. (yes its the first article of 2015 on the blog). There were differences between the groups. Which is about as much as I can say about head MRI, the mean diffusivity was lower in the intervention group. Which is good, apparently. In just about every region of the brain there were significant differences in what I shall from now on refer to as MD, as if I knew what I was talking about. So give more food. It makes the babies grow better, including their head, and it improves their MD, which is a good thing to do.
    3 points
  39. Necrotizing Enterocolitis remains a devastating disease. One of the major causes of mortality in Very Low Birth Weight Infants, it often strikes when babies are starting to do well. Because it is relatively unpredictable, observational studies are potentially useful, but can easily be misleading. In particular, observational studies which are performed as a result of a perceived change in incidence might easily be biased. One recent study that was published has received some publicity, I myself received some links on Linked-In pointing to this study, which at first sight seems to show that advancing feeds slowly might decrease NEC. Lets examine the data a bit more carefully. In 2009 a hospital changed their feeding policies. A paper published in 2014 reported their data from 2009 to 2012. According to the published article the paper was received on July 24th 2014, and accepted on August the 5th. Which immediately makes me wonder two things, why the authors decided to perform this study, and how do they get a paper accepted so quickly? If the authors performed the study because they saw a decrease in NEC, and then decided to do the analysis, that immediately creates a bias, many other hospitals could possibly have made a similar change and not noted any change in NEC, and therefore not looked at their data. Studies such as this are more likely to be reliable if the decision to prospectively collect and try to publish their data is made at the time that the change in therapy is introduced. But then a similar study showing no effect on NEC would be very difficult to publish, and probably not be accepted in under 2 weeks! There are a couple of concerning things in their findings, one is that after the change in the protocol there was not actually statistically any less NEC overall than before the change in protocol. Only by a subgroup analysis, was the group of babies under 750g significant, and then they did not report the p-value of the interaction, which is really essential. They showed much less NEC in the babies under 750 g birth weight than those between 750 and 1000g. Which really strongly suggests to me that this is just the result of the random nature of NEC incidence, I don't know any large study that has ever found more NEC in the larger babies. More worryingly, the new protocol led to babies having later commencement of feeds, longer use of intravenous nutrition, longer use of picc lines, and really horrendous nutritional outcomes, with over half of the babies being under the 10th percentile at discharge (admittedly that was better than the 75% with their older protocol). The feeding protocol that they introduced is entirely non-evidence based, as I have noted before here, there is no evidence from controlled trials that varying the advancement of feeds has any effect at all on the incidence of NEC. A slightly older study (from 2009) provides interesting data from the German Neonatal Network, and is, I think, much more reliable. They compared the outcomes of babies from centers where it took on average less than 12.5 days to get their VLBW babies on full feeds, to centers where it took on average more than 12.5 days to get the babies to full feeds. You can see here the clinical outcomes from the study. The only things that were different between the groups were the late-onset sepsis, which was much higher in the babies with slower feeding. Surgical NEC was slightly (non-significantly) more frequent with slower feeding, and severe retinopathy was also higher, which is entirely consistent with the recent information linking retinopathy with poorer nutrition.
    3 points
  40. One of Annie Janvier's first research projects was a case control study of the influence of prophylactic indomethacin on intestinal perforations. Under my supervision she analyzed cases of spontaneous intestinal perforation (SIP), and we analyzed the influence of prophylactic indomethacin, which was highly significantly related. As we knew at the time, there are numerous biases in this type of research. For one, we decided to do the study because we had just had a run of SIP; often such studies are stimulated by just this kind of phenomenon. Which immediately introduces bias: what you should probably do, if you have a cluster of adverse outcomes, is to take your suspicions and analyze data from a completely independent data set, of which you are not a part. But few of us have access to such data. We had recently introduced indomethacin prophylaxis, and had this run of SIP, so the analysis did show an associations between the 2, which made us worry, but we certainly weren't convinced that the association was causal, nor that our data were free of bias. As an aside, Annie, a fellow at the time, was really pissed off when a well known senior researcher, who shall remain nameless, walked past her poster and sniggered. Don't do that folks (most of my good friends and colleagues wouldn't dream of it): even if there are flaws in the research, we should encourage junior people to be thoughtful, to try and analyze their experiences and find ways to ask and answer questions. That is a long introduction to a new publication from the NICHD database. And another beef, is it really necessary, when someone does an analysis of the NICHD database, that there are 19 authors? Did all 19 have a substantial intellectual contribution to this work? Or is it more of a little present thrown to the waiting hordes, a sort of quid pro quo, you scratch my data, I'll scratch your CV? Just asking. Kelleher J, et al, et al, et al. Prophylactic Indomethacin and Intestinal Perforation in Extremely Low Birth Weight Infants. Pediatrics. 2014. This prospective cohort comparison used the generic database to examine the incidence of SIP in babies who received prophylactic indomethacin or not, and subdivided each group as to whether they had early feeding or not. Early feeding was defined as receiving any feeds in the first 3 days of life. My European readers might laugh at that as a definition of early feeding, but there were plenty of these babies, 400 to 1000 g birth weight, who were npo for at least 3 days, indeed there were 11,000 of the 15,000 who got no enteral feeding during the first 3 days (between 1999 and 2010). As for the results, there was no evidence that prophylactic indomethacin increased SIP, and early feeding is associated with a lower rate (there may be some confounding here, as babies who have abdominal signs and maybe early signs of SIP might have feeds held as a result). Babies who had early feeding had less developmental delay at 20 months, (or, as the NICHD persists in calling it, 'neurodevelopmental impairment': if I have to say it again, a low Bayley score is not an impairment!) and the association of early feeding with better Bayley scores, was seen whether or not the babies got prophylactic indomethacin. The prophylactic indomethacin babies also did not have more NEC, and they had fewer PDA ligations. They also had much less frequent treatment with indomethacin or ibuprofen later in their hospital course, but the RR is reported as being over 1, and significant, which I don't understand. The early enteral feeds groups also had much quicker advancement to full feeds, and many fewer days of parenteral nutrition. This confirms the RCT results, with a lot more babies but an observational study design, indomethacin doesn't seem to increase SIP (despite our case-control findings) decreases PDA ligations, and adds very positive data about early feeds, at least starting feeds before 3 days of age. I think you should have a very good reason for not feeding a very preterm baby, such as shock requiring inotropes perhaps.
    3 points
  41. Call me prescient, OK, you won't, but I will. Two recent observational studies suggest that the recent NICE guidelines have had adverse effects on infants evaluated for potential early neonatal sepsis. 'NICE' of course is not an adjective for how good the guidelines are, but the acronym for the National Institute of Health and Care Excellence in the UK. Any long time neonatalresearch watchers will remember vividly my perceptive analysis and critique of those guidelines. Which included the good (to stop antibiotics at 36 hours if no signs of sepsis) and the questionable; universal measurement of CRP at the start, with a repeat at 18 to 24 hours, and stopping the antibiotics if the trend is 'reassuring'. My concern being that CRPs are relatively sensitive but with low specificity. Infants exposed to many different stressors, infectious and not, may have increased CRP. As early onset sepsis in term infants is relatively uncommon in most of the at-risk situations outlined, the proportion of babies who have unnecessary prolongation of antibiotic therapy solely for a CRP which is not 'reassuring' might be substantial. You have, of course, to balance that against the theoretical benefit of continuing antibiotics in an infant who is truly septic, in whom the antibiotics would have been stopped were it not for the non-reassuring CRP. A benefit which is likely to occur much less often. Two recent studies have sought to quantify these impacts. Mukherjee A, Davidson L, Anguvaa L, Duffy DA, Kennea N. NICE neonatal early onset sepsis guidance: greater consistency, but more investigations, and greater length of stay. Archives of Disease in Childhood - Fetal and Neonatal Edition. 2014. This is a before-after study which investigated the impacts on babies evaluated for possible sepsis. I think this is from a single hospital in London (it is a short report so some details are missing, also weirdly there is not a single reference, not even to the NICE guidelines), and it appears that about 8-9% of babies had sepsis work-ups, with around 70 babies affected in each of the 2 month cohorts, before and after the NICE guidelines. They looked at how many babies stayed in the hospital less than 72 hours, this decreased from 38.1% to 18.4%. More babies stayed over 5 days, from 20.9% up to 27.7%. They found that 58% of the repeat CRPs were used to change management, including leading to more LPs (14% up to 23%). In all of their babies there were no positive cultures. We envisaged shorter hospital stays with new NICE standards, particularly, with the aim of 36 h blood culture reporting. However, repeat CRP led to further investigations, increased LPs and longer durations of treatment and stay. This, in turn, impacted on workload and cost, and influenced parental experience in the first few days of life Naydeva-Grigorova T, Manzoor A, Ahmed M. Management of early-onset neonatal infections. Archives of Disease in Childhood - Fetal and Neonatal Edition. 2014. This experience, published as a letter in Archives, recounts what happened with about 40 babies, before and after the guidelines. 1 of 40 before the guidelines had an LP, compared to 8 afterward. Entirely because the CRP was raised. Hospital stay increased after the guidelines, and duration of antibiotic use increased. None of the babies had positive cultures. Our results indicate that babies in group B had prolonged hospital stay requiring longer duration of intravenous antibiotics without much clinical benefit. I think there should be a rapid re-evaluation of these guidelines, which seem to be only having negative effects, at least from these 2 experiences. I think the reason that the NICE guidelines are not very nice is that the data being used to support the recommendation are based largely upon a single study from 1998, a good study from Bill Benitz in California, unfortunately (for the NICE guidelines) that study was not among asymptomatic babies, but only babies who had symptoms, the list of which includes shock, new apnea, lethargy, respiratory distress and so on, and also includes preterm infants down to 550 grams birth weight. It only included babies treated for sepsis in one of 3 NICUs. (See evidence table 10.3 in the guideline that you can find here). So it is of no relevance to the healthy full term baby with risk factors alone, in whom the false positives are clearly going to be much more frequent. In the more recent study by Thierry Lacaze and colleagues, which only included asymptomatic infants being evaluated because of signs of sepsis, a single CRP at 18 hours of age had a PPV of 14% for proven or probable sepsis. I discussed the article when it first came out, and I think the suggestion of those authors, that a low CRP at 18 hours of age, using a method which gave a result immediately to the medical team, could lead to earlier stopping of antibiotics and earlier discharge is reasonable. The implication being that a non-reassuring CRP would then mean waiting until 36 hours and making a decision independent of the CRP. For asymptomatic babies CRPs are too sensitive, being elevated for all sorts of reasons unrelated to sepsis requiring treatment.
    3 points
  42. Neil Marlow has published a thoughtful, and thought provoking, article to address the issue outlined in the title. What are the appropriate outcomes when designing neonatal research studies? It has become almost a rule, that a multi-center trial of an intervention in neonatology, especially if it is planning to enroll very preterm infants, has to have 'survival without neurological or developmental disability' as the primary outcome, with the 'disability' part measured at about 2 years. There is some value to this outcome, very preterm infants have high mortality and high morbidity in those domains, infants who die cannot be developmentally delayed, so they are competing outcomes that need to be taken into account if we are trying to construct a dichotomous end-point. Like most things in trial design we have to make compromises, later follow up might be nice, but it will increase costs and increase drop-out rate; follow up to 2 years allows good retention rates, if you work hard at getting parents to return, but means you need to use developmental screening tools which are developed for very young infants. There are however, numerous problems with this approach, which are discussed in this piece. (Marlow N. Is survival and neurodevelopmental impairment at 2 years of age the gold standard outcome for neonatal studies? Archives of Disease in Childhood - Fetal and Neonatal Edition. 2014). I also think we do need to rethink this approach for some of the following reasons (which overlap with the reasoning of Neil Marlow) 1 Developmental delay is not a dichotomous outcome. It is convenient for research planning to think of children either having impairment or not, but of course, developmental delay is a continuum, arbitrarily deciding that a Bayley score of 69 is delayed, but a score of 71 is not, misses all sorts of nuances in outcomes. 2. Developmental delay is not stable over time: many children labelled as delayed at 2 years have intellectual abilities in the long term that are close to, or above, average (in fact according to the work of Maureen Hack, 2/3 of them do). The improvement in developmental scores is correlated more closely with social advantages than to anything which occurs in the neonatal period. 3. Developmental delay has little or no influence of quality of life. Children with developmental delay can, and usually do, have an excellent QoL. If the purpose of your research project is to decided which therapies we should use in the future, then whether or not the therapy affects quality of life should be our main consideration, but as far as I know, no therapy has been shown to affect quality of life, apart from effects on quantity of life. In other words, surfactant for RDS increases quality of life, because more children are alive to have a life of good quality! 4. Very few neonatal preterm studies have ever shown an effect on neurological impairment or developmental delay. Of all the studies in the very preterm baby, which have actually been confirmed to reduce developmental delay? Maybe someone should do a systematic review to answer that question, of the top of my head there is Caffeine (at least when defined by developmental screening at 2 years, but not when examined at 5 years), and then there is... well that's about it. So many of our decisions about which treatments are proven to be beneficial are really based on their impacts on survival, or on other morbidities, such as lung injury (another non-dichotomous outcome that we 'dichotomize' for facilitating compound outcomes). 5. Another important consideration is that the effect of an intervention on survival and on neurological or developmental outcomes may be in different directions. Which means that a trial might be 'negative' but still have important results that should change practice. I don't know if this has happened for the outcome of survival and 2 year developmental screening test scores, but it is analogous to what SUPPORT showed. SUPPORT was a negative trial. The composite primary outcome (survival without severe retinopathy) was not affected by different saturation target ranges, because the impacts on the two components of the outcome were in opposite directions. Neil Marlow includes a discussion of the TIPP trial, which showed a reduction in severe brain injury, a reduction in serious pulmonary hemorrhage, and a reduction in need for PDA ligation. But, the study did not show an overall improvement in developmental outcomes with indomethacin prophylaxis compared to control. I think it was an excellent trial with reliable results, but because of the lack of improvement in the primary outcome it has discouraged the use of prophylactic indomethacin. However, there was a reduction in severe hemorrhage from 13 to 9%: if the only effect of indomethacin on the brain or on development was the reduction in IVH, and if the patients who had a severe IVH had an increase in neurodevelopmental 'impairment'; then any benefit would only have been on those 4% who escaped IVH, and the impact on the scores of the groups as a whole would have been very small. This study was therefore grossly underpowered, in the sense that it would not be able to show that a reduction in severe IVH of that magnitude had an overall effect on the developmental scores of the entire group. In their answer to an article which questioned why prophylactic indomethacin was not more widely used, De Mauro et al stated " TIPP failed to demonstrate any long-term benefit of indomethacin prophylaxis, but the study also failed to prove the absence of long-term harm'' Which is true, but I would say it is not the whole story, because you could equally well say, ''TIPP failed to prove the absence of long term benefit, but the study also failed to demonstrate any long-term harm '' A study with no statistically significant overall effect on developmental outcome always means that there is some possibility that developmental outcomes are actually improved, or actually harmed, depending on the range of the confidence intervals of the result. TIPP gives some confidence that developmental outcomes are not dramatically harmed by indomethacin, but there will also be a possibility that in reality there is some impact on development: the confidence intervals of the study result gives us a range within which we can say, with 95% confidence, the true difference in the means of the Bayley scores lie. Uncertainty has been reduced by doing the trial, it means it is likely that the true impact on the Odds of an infant (similar to those eligible for the trial) having a Bayley score below 70 are between an Odds ratio of 0.8 and 1.4 if they receive prophylactic indomethacin rather than not. Or, to put it in terms that I find easier to conceptualize, the risk of having a Bayley score below 70 is probably (with 95% confidence) between a 17% reduction and 29% increase in risk, if you get prophylactic indomethacin. If most survivors of NICU do well (as they do) and almost all have a good quality of life (which they do) and the history of neonatal intensive care research has shown it is extremely difficult to demonstrate improved developmental outcomes at 2 years (as I discuss above); and developmental outcomes at later ages than that (when testing is more relevant for functional ability) have never been affected by a neonatal intervention, then maybe we should reconsider our outcomes. I think that trials should be designed and powered to examine effects on improving survival and other serious short term complications, such as severe cerebral hemorrhage, necrotizing enterocolitis and so forth, and that surveillance for other medium and long term outcomes, including developmental screening test scores, should be considered important for ensuring safety. I also think we should be asking parents about these things. Is a reduction in severe brain hemorrhage an outcome that they think is important, even if we can't prove an advantage in terms of Bayley scores? Which is all very similar to what Neil Marlow says in his article. So he must be right.
    3 points
  43. The story around cord management after birth continues to be an evolving one. I have certainly posted my own thoughts on this before with my most recent post being Delayed cord clamping may get replaced. Time for physiological based cord clamping. While this piece demonstrated that there are benefits to longer times till clamping is done, it also showed that if you go too long hypothermia becomes a real risk and with it possible complications. At least in our centre the standard that we have tried to reach is DCC for one minute for our infants. As you will no doubt know from the literature reviewed here before, this is likely not long enough! One or Three Minutes? This study caught my eye this week. Effect of early versus delayed cord clamping in neonate on heart rate, breathing and oxygen saturation during first 10 minutes of birth – randomized clinical trial What struck me in particular about this paper was not just the physiologic outcomes it was looking at. What is remarkable is the size of the study. So many articles that are published in Neonatology have under a hundred patients. On occasion we see studies with hundreds. In this case the authors included 1510 patients who were randomized to early ≤60 s of birth and ≥ 180 s for time of clamping. What is also interesting here is that early which used to be considered right after delivery of the infant is now 1 minute in this study. I like that this is the accepted new norm for this type of study. Inclusion criteria were such that these were all low risk vaginal deliveries with fetal heart rate (FHR) ≥100 ≤ 160 bpm and all infants were ≥33 weeks. Although 1510 were randomized (power calculation for sample size found there should be 566 per group based on an expected loss of 25% per arm. In the end there were 670 in the ECC and 594 in the DCC groups that adhered to the protocol. In the ECC group the mean duration of time till clamping occurred was 31.2 s (+/-14.4) vs 198.5s (+/-16.9). The Results The goal after delivery is to increase blood flow to the lungs as PVR drops. In order to do so this requires adequate ventilation but it also requires adequate perfusion of the myocardium. If you clamp too early and pulmonary blood flow has not yet increased you run the risk of having a sudden drop in coronary blood flow with oxygenated blood from the placenta and with that bradycardia. A longer time on “heart lung bypass” from the placenta should allow for a smoother transition. That is what was seen here. At 1, 5 and 10 minutes infants randomized to the DCC had better oxygen saturations. Heart rates interestingly were lower in the DCC group but that could also be related to better oxygenation leading to less compensatory tachycardia. In other studies in which the cord was clamped immediately bradycardia was more common. This difference here may reflect timing of the clamp on heart rate. Lastly, time to first breath was much faster in the group randomized to DCC. Might this be an effect of better oxygenation? What they didn’t measure? There was no comment on risk of hypothermia or other markers of illness such as rates of admission to NICU, hypoglycemia, lethargy or other markers of an infant who became cold. If this is to become standard practice measures need to be in place to prevent these concerns from becoming reality. It is also worth noting the population studied. These are healthy late preterm and term pregnancies. More work is needed on younger infants and those with risk factors in pregnancy. How would mothers with poor tracings, diabetes or hypertension fare as well as those who have growth restricted infants? This field is growing and I will continue to follow this evolving story and share information as it becomes available. One thing in my mind is fairly certain though and that is that clamping right after delivery for routine births should be a thing of the past.
    2 points
  44. I have written about non-traditional methods of providing surfactant to newborns previously. The practice of intubating a preterm infant to administer surfactant and leaving the endotracheal tube in with a slow wean of ventilation is mostly a thing of the past (at least in my units). Strategies have evolved and have seen the development of the INSURE technique, LISA methods, use of an LMA to delivery surfactant and even simple deposition into the pharynx all with variable success. The Holy Grail To me at least, the Holy Grail of surfactant delivery has been aerosolization. A small non randomized study was done in by Finer et al in 2010 An open label, pilot study of Aerosurf® combined with nCPAP to prevent RDS in preterm neonates. This study noted a reduction in CPAP failure with nebulized surfactant but as a pilot was not large enough to move the needle. Since then the Cochrane group weighed in and declared that there was not enough evidence to support the practice. The CureNeb group anchored by Dr. Pillow though has now published a double blind RCT entitled Nebulised surfactant to reduce severity of respiratory distress: a blinded, parallel, randomized controlled trial. It certainly sounds interesting and might help determine if the needle has indeed moved. The Study Poractant alfa at 200 mg/kg was used in this study and delivered via aerosolization using a vibrating membrane called the eFlow. The authors chose to look at infants from 29 0/7 to 33 6/7 weeks at birth and stratified them into two groups of 29 0/7 to 31 6/7 and 32 0/7 to 33 6/7 weeks. They estimated a need for 70 babies based on an anticipated failure rate of 30% in the control group vs 5% in the treatment group. Unfortunately, due to several reasons the study was only able to recruit 64 babies for randomization before being stopped due to the recruitment issues. The design of the study included adequate blinding with a sham procedure and there were predefined “failure criteria” necessitating intubation at the outset of the study. These criteria are acceptable to me as they are similar enough to my own practice and were: 1. FiO2 >0.35 over more than 30 min OR FiO2 >0.45 at anytime. 2. More than four apnoeas/hour OR two apnoeas requiring bag and mask ventilation. 3. Two capillary blood gas samples with a pH <7.2 and partial pressure of carbon dioxide >65 mm Hg (or partial pressure of carbon dioxide in arterial blood (PaCO2) >60 mm Hg if arterial blood gas sample). 4. Intubation deemed necessary by the attending physician. What did they find? The primary outcome CPAP failure within 72 hours of birth was indeed different in the two groups. CPAP failure by 72 hours CPAP + surfactant 11/32 (34%) CPAP 22/32 (69%) (RR (95% CI)=0.526 (0.292 to 0.950)) Clearly the event rates were quite off from what they expected in the power calculation but given that they found a difference as opposed to no difference at all the fact that they didn’t recruit the numbers they planned is of less importance. However, what is interesting is when they looked at the planned analysis by stratification an interesting finding emerged. Group 1 (29 0/7 to 31 6/7) CPAP failure by 72 hours CPAP + surfactant 12/21 (57%) CPAP 12/19 (63%) (RR (95% CI)=0.860 (0.389 to 1.90)) Group 2 (32 0/7 to 33 6/7 CPAP failure by 72 hours CPAP + surfactant 1/11 (9%) CPAP 10/13 (77%) (RR (95% CI)=0.254 (0.089 to 0.727)) There were a number of secondary outcomes looked at as well which may be of interest to you but as the numbers here are quite small I will not comment other than to say there was no increased incidence of complications with surfactant administration in this fashion. Also for those who ultimately failed CPAP the time when they did so was quite delayed compared to CPAP alone. Age at intubation for nCPAP failure, hours 4.9 (2.7–10.6) 11.6 (9.0–31.1) 0.008* What can we take from this? I believe these results are encouraging even if the study is a small one. The message I take from this study is that aerosolization of surfactant delivers some amount of product to the lungs. Those with more significant RDS or smaller lungs (those in the 29 0/7 to 31 6/7 group) may not get enough surfactant to treat their RDS sufficiently to avoid intubation. Those with less significant RDS or a larger number of alveoli get “enough” of a dose delivered to the alveoli to make a difference and avoid intubation. It is worth stressing that there can be no specific comment about using this strategy in even more immature infants as they weren’t tested. If I had to guess though, I would expect no difference given the findings in the smaller group. As a physician responsible for transport though I am interested in the potential benefits to those born in non-tertiary centres. Many centres lack individuals with the confidence and skill to regularly place endotracheal tubes. For these centres it may be that providing nebulized surfactant could delay the time to treatment failure, allowing more time for a trained transport team to arrive. Training of course would be needed in these centres on how to administer surfactant in this way but it is an interesting concept to consider. With a near tripling of the average time to treatment failure the extra hours on CPAP would be much appreciated when weather delays or difficulty securing air assets means long delays in transport team arrivals. To be sure this isn’t the last study of this kind but it certainly is an interesting start and one that will no doubt produce questions that will help formulate the next study design.
    2 points
  45. The medical term for this is placentophagy and it is a real thing. If you follow the lay press you may have seen that originally this was promoted by Kourtney Kardashian who did this herself and then by Kim who planned on doing the same after delivery. See Did Kourtney Kardashian Eat Her Placenta? This is not completely without basis as many readers will be thinking already that they have heard about the health benefits of doing the same. Reports of improved mood and reductions in the baby blues following ingestion of placenta as well as improvements in breast milk production have led to this growing practice. The evidence for this up until recently though was quite old and fraught with poorly design of such studies. The bigger driver however has been word of mouth as many women having heard about the promises of better mood at the very least have thought “why not? Can’t hurt.” What I will do in this post is run through a little background and a few recent studies that have shed some light on how likely this is to actually work. Where did the idea come from? Animals eat their placentas after delivery. It turns out that unprocessed placenta is quite high in the hormone prolactin which is instrumental for breastfeeding. Given the large amount of this hormone as well as the number of other hormones present in such tissue it was thought that the same benefits would be found in humans. Eating unprocessed human tissue whether it is put in a capsule or not is unwise as unwanted bacteria can be consumed. In fact, a case of GBS sepsis has been linked to such a practice in which the source of the GBS was thought to be due to contaminated unprocessed maternal placenta that had been ingested. Buser GL, Mat´o S, Zhang AY, Metcalf BJ, Beall B, Thomas AR. Notes from the field: Late-onset infant group B streptococcus infection associated with maternal consumption of capsules containing dehydrated placenta. What happens when you process placenta by steaming and drying? This would be the most common way of getting it into capsules. This process which renders it safe to consume may have significant effects on reducing hormonal levels.This was found in a recent study that measured oxytocin and human placental lactogen (both involved positively in lactation) and found reductions in both of 99.5% and 89.2%, respectively compared versus raw placenta. I would assume that other hormones would be similarly affected so how much prolactin might actually wind up in these capsules after all? Clinical Randomized Double Blind Controlled Trial Twenty seven women from Las Vegas were recruited into a pilot trial (12 beef placebo vs 15 steamed and dried placenta) with the authors examining three different outcomes across three studies. The first study Effects of placentophagy on maternal salivary hormones: A pilot trial, part 1 looked at a large number of salivary hormones at four time points. Plasma samples were taken as well to determine the volume of distribution of the same. First samples were at week 36 of gestation then within 4 days (96 h) of birth followed by days 5–7 (120–168 h) postpartum and finally Days 21–27 (504–648 h) postpartum. All consumption of capsules was done in the home as was collection of samples. As per the authors in terms of consumption it was as follows “two 550 mg capsules three times daily for the first 4 days; two 550 mg capsules twice daily on days 5 through 12, and then to decrease the dose to two 550 mg capsules once daily for the remainder of the study (days 13 through approximately day 20 of supplementation). Outcomes No difference was found between salivary concentrations of hormones at any time point other than that with time they declined following birth. Curiously the volume of distribution of the hormones in serum was slightly higher in the placenta capsule groups but not enough to influence the salivary concentrations. It was felt moreover that the amount of incremental hormone level found in the serum was unlikely to lead to any clinical response. The second study was on mood Placentophagy’s effects on mood, bonding, and fatigue: A pilot trial, part 2. Overall there were no differences for the groups but they did find “some evidence of a decrease in depressive symptoms within the placenta group but not the placebo group, and reduced fatigue in placenta group participants at the end of the study compared to the placebo group.” The last paper published from the same cohort is Ingestion of Steamed and Dehydrated Placenta Capsules Does Not Affect Postpartum Plasma Prolactin Levels or Neonatal Weight Gain: Results from a Randomized, Double-Bind, Placebo-Controlled Pilot Study. This study specifically addressed the issue of prolactin levels and found no difference between the groups. Neonatal weight gain was used as a proxy for breastmilk production as it was thought that if there was an effect on breastmilk you would see better weight gain. About 80% in both groups exclusively breastfed so the influence of formula one can’t take out of the equation. In the end weight gain was no different between groups although a trend to better weight gain was seen in the placebo group. To eat or not to eat that is the question? What is clear to me is that the answer to this question remains unclear! What is clear is that I don’t think it is wise to consume raw placenta due to the risks of bacterial contamination. Secondly, the levels of hormones left in the placental preparation and the most common preparation of steaming and drying leave hormone levels that are unlikely to influence much at all from a biochemical standpoint. It also seems that breastmilk production and neonatal weight gain aren’t influenced much by consumption of these pills. The issue though in all of this is that while the previous research was of low quality, the current research while of better quality is at a low volume. These were pilot trials and not powered to find a difference likely. The finding in the subgroup of some effect on mood at the end of the study does leave some hope to those that believe in the power of the placenta to help. Would a larger study find benefit to this practice? My suspicion from a biochemical standpoint is not but that one may feel a benefit from a placebo response. Should you go out and have your placenta prepared for consumption? If you have Kardashian like wealth then go for it if you think it will help. If you don’t then I would suggest waiting for something more definitive before spending your money on placentophagy.
    2 points
  46. Excited for my first speaker oportunity to a peds audience.We a small group of about 20 I did expect a litlle more. The good Things and not so good that needed improving here. The conference wad set to be the first consist of primary care topics & community health. The second was solid peads with a special section of neonatology talks in the afternoon. The was also a poster competition in the mix. Lets start with the good I really enjoyed the networking oportunity over a nice healthy lunch with people. We happened most to NICU peps of bar various multidisciplinary backgrounds so we got talking about developmental outcomes of preemie at several stages. Thus we able to cross pollinate with ideas. The were several talk that were really relevant to my posdoc expecially organisation:community health better and those that NICU ones .The most thought provoking one was the method of management explained by the Arizona Prof. McGrath ,developmental psychologist working NICU on neonatal abtinense sindrome: how they reduced the stay to about weekish-ten days reduced the used of morphine derivates. Other talk were little lenghty. Personal I manage to give my talk to the small peds audience. I was a tad nervous but manage to give a somewhat seamless talk summary a few points as it overlap with the previous talk on the golden hour on my work in ethics in NLS and generate some debate with those in room. I glad that my hotel was close by 10 walks away. A bonus on get macarons for mum on way back at the airport at Orly. On the otherhand, the organization of the event needed improving as it was a bit ad hoc from my experience organising .We totally underestimated how far it would be from the airports CDG and Orly : +2 hours using a mix public transport , I used my trusty app citymapper to get there.The conference site was a cute Holiday Inn @ Noisy le Grand, subburds well outside Paris .
    2 points
  47. A 28 week preterm infant now two weeks of age develops bilious emesis and abdominal distension. An x-ray reveals an intestinal perforation and surgery is consulted. Arrangements are made to go to the operating room for a laparotomy and due to apnea and hypotension the baby is both intubated and placed on dopamine. The resident on service ensures that blood is available in the operating room and an hour after presentation the baby is found to have a HgB of 102 g/L with a HcT of 35%. I don’t know about you but if I am then asked whether we should give blood now or in the OR I might say at that level with the degree of illness to give blood or I might say wait till the baby gets to the OR if perhaps they were fairly stable on the support. You the reader might be more convinced of your actions but if I manipulate the numbers a little bit to say 105 g/l and HcT of 37% might you feel different? What about 110 g/L and 39%? You get the picture. Where is that magic cutoff where we say prior to an OR that a baby needs blood or can wait? In our heads of course we conjure up the equation for delivery of O2 to tissues Cardiac output X (1.39 X HgB X Sat +0.003*pO2) and realize that the delivery of oxygen is critically dependent on HgB level but how much is enough? The truth is I don’t think we really know but we do a good job of coming up with some markers such as lactate or more recently near infrared spectroscopy to give us an idea of how much O2 the tissues are seeing. How much HgB does a baby need before surgery? Although this may seem like something that is well known, the truth is we don’t really know. We may have an inkling though based on a recent paper entitled Association of Preoperative Anemia With Postoperative Mortality in Neonates by S. Goobie et al. They performed a retrospective review of a US surgical quality database to examine mortality after operations and identified 2764 neonates out of 114395 children who underwent surgery. Similar to previous studies the neonatal postoperative mortality rate was higher at 3.4% than the rest of childhood at 0.6%. When examining the effect of low hematocrit prior to surgery they further identified a cutoff of 40% below which the risk of mortality increased. Of the neonatal group that survived 31% had a preop hematocrit of 40% or more while of those who died 72% had a hematocrit < 40%. Hematocrit was not the only factor predicting mortality though as ASA class 3 – 5 (an anesthesiology risk score where these scores indicate severe systemic disease or emergencies), weight < 2 kg, preoperative ventilation and inotropic support. Put simply, sicker small patients have worse outcomes which I suppose should not surprise anyone. So how do we interpret this data? One important point that this article does not control for is the specific type of condition that the patient had. Clearly all conditions of the newborn are not the same as for example an umbilical flap closure of gastroschisis compared to fulminant necrotizing enterocolitis. The authors do try and control somewhat for this by demonstrating that the ASA categories demonstrate if you have severe systemic disease you are worse off but where does this leave the hematocrit? The other possible explanation is that the anemia is simply a reflection of the critical nature of the patient. Sicker patients are more likely to be anemic and also patients who present later are as well. A baby needing a colostomy for a bowel obstruction diagnosed after birth is likely to have low risk of mortality and also have a normal HgB. Contrast this with the baby who develops NEC at 3 weeks of age who is likely anemic or close to being so when they present and in the presence of shock and DIC becomes even more so. Is the low HcT just a proxy for severity of disease? I suspect for the otherwise well infant who is electively intubated for surgery, having a hematocrit alone below 40% is not dangerous. What do we do though with the baby who is on inotropes for example. To truly answer this question we need a randomized controlled trial comparing transfusing patients with a hematocrit below 40% vs choosing a higher threshold of say 50% to say whether it makes a difference. That doesn’t help us though in the here and now. This gold standard for studies won’t tell me what to do for a few years but right now I have to decide what to do for a patient in front of me. Not everyone may agree with me on this but I think in such circumstances I would transfuse based on this publications results. To the naysayers out there I would suggest that whether I choose to give the blood or not before the operation, they will be getting it after they enter the OR. Why not give them a boost before they undergo the knife? It is not a question of whether they will be transfused or not it is a difference in time. If I have the chance I will “top them up” but what will you do?
    2 points
  48. To many of you the answer is a resounding yes in that it reduces stress. Why is that though? Is it because you have had a personal experience that has been favourable, it is the practice in your unit or it just seems to make sense? It might come as a surprise to you who have followed this blog for some time that I would even ask the question but a social media friend of mine Stefan Johansson who runs 99NICU sent an article my way on this topic. Having participated in the FiCare study I realised that I have a bias in this area but was intrigued by the title of the paper. The study is Parental presence on neonatal intensive care unit clinical bedside rounds: randomised trial and focus group discussion by Abdel-Latif ME et al from New Zealand and was performed due to the lack of any RCTs on the subject specifically in the NICU. Before I go on though I have to disclose a few biases. I love parents being on rounds so I can speak with them directly and have them ask me any questions they may have after hearing about their infants condition. Our unit encourages the practice. We are rolling out the principals of FiCare after being part of the study which encourages parental presence at the bedside for far more than just rounds.For information on implementing FiCare click here While this study is the only reported RCT on the subject in the NICU, the FiCare results will be published before long. What is the problem with having families on rounds? The detractors would say that sensitive information may be more difficult to discuss out in the open for fear that the family will take offence or be hurt. Another concern may be that teaching will be affected as the attending may not want to discuss certain aspects of care in order to prevent creating fear in the parents or awkwardness in the event that the management overnight was not what they would have done. Lastly, when patient volumes and acuity are high, having parents ask questions on rounds may lead to excessive duration of this process and lead to fatigue and frustration by all members of the team. So what does this study add? This particular study enrolled 72 families of which 63 completed the study. The study required 60 families to have enough power to detect the difference in having parents on rounds or not.The design was interesting in that the randomisation was a cross over design in which the following applied. One arm was having parents on rounds and the other without. The unit standard at the time was to not have parents on rounds. ≤30 weeks 1 week in one arm, one week washout period then one week in the other arm >30 weeks 3 days in one arm, three day washout and then three days in the other arm The primary outcome was to see if there would be a significant difference in the Parental Stressor Scale. Surprisingly there was no difference across any domains of measuring parental stress. When we look at questions though pertaining to communication in the NICU we see some striking differences. The families see many benefits to the model of being on rounds. They appear to have received more information, more contact with the team, contributed more to the planning of the course of their babies care and been able to ask more questions. All of these things would seem to achieve the goals of having parents on rounds. So why aren’t parents less stressed? This to me is the most interesting part of this post. The short answer is I am not sure but I have a few ideas. The study could not be blinded. If the standard of care in the unit was to not have parents on rounds, what kind of conversations happened after rounds? Were staff supportive of the families or were they using language that had a glass is half empty feel to it? Much like I am biased towards having parents on rounds and thanking them for their participation were there any negative comments that may have been unintentional thrown the families way. Is a little knowledge a dangerous thing? Perhaps as families learn more details about the care of their baby it gives them more things to worry about. Could the increase in knowledge while in some ways being pleasing to the family be offset by the concern that new questions raise. Was the intervention simply too short to detect a difference? This may have been a very important contributor. This short period of either a week or two leaves the study open to a significant risk that an event in either week could acutely increase stress levels. What if the infant had to go back on a ventilator after failing CPAP, needed to be reloaded with caffeine or developed NEC? With such short intervals one cannot say that while communication was better the parents were not stressed due to something unrelated to communication. In an RCT these should balance out but in such a small study I see this as a significant risk. So where do we go from here? I applaud the authors for trying to objectively determine the effect of parental presence on rounds in the NICU. Although I think they did an admirable job I believe the longer time frame of the FiCare study and the cluster randomised strategy using many Canadian centres will prove to be the better model to determine effectiveness. What the study does highlight though in a very positive way is that communication is enhanced by having parents on rounds and to me that is a goal that is well worth the extra time that it may take to get through rounds. Looking at it another way, we as the Neonatologists may need to spend less time discussing matters after rounds as we have taken care of it already. In the end it may be the most efficient model around!
    2 points
  49. Does being rude stimulate people to do better, or does it have adverse effects on performance, and team functioning? And how to prove it on way or another? This really interesting, innovative paper from a team in Israel has performed an RCT to address the problem. Riskin A, et al. The Impact of Rudeness on Medical Team Performance: A Randomized Trial. Pediatrics. 2015. The authors created 24 NICU teams and arranged for them to receive some comments from a supposed visiting expert from the USA. Half of them included some mildly rude comments, which the team received either just before or midway through a simulated resuscitation of a newborn manikin. Just before the simulation, to the rudeness exposed group, the "expert" stated that he was "not impressed with the quality of medicine in Israel". Ten minutes later the simulation was stopped and the participants heard that "medical staff like those observed wouldn’t last a week in his department". He added that he "hoped that he would not get sick while in Israel". The study found substantial negative effects of what they refer to as "mild incivility" on both diagnosis of problems during the simulation and on procedural performance. For example the subjects were much less likely to correctly verify the position of a tube when they had been the target of the rudeness. They also showed that the rude comments affected information sharing within the team, and on whether the team members sought help from each other. I must say I have been exposed to rudeness, sometimes much more direct and biting than the comments in this research, at many times during my career, and have, to be honest, also occasionally been rude to others myself. Sometimes a transient irritation or annoyance can lead to comments or attitudes that are negative and to "incivility". In a very high stress environment like the NICU, making snarky comments when things don't go well is a common reaction. I think that we should all try even harder to avoid such responses, not just because they may hurt feelings and harm morale, but because it actually looks like they can have adverse effects on the medical care that our patients receive.
    2 points
  50. It sounds simple, but actually it turns out to be very complicated and controversial. The question is are we improving our NICU ? Has our NICU performance remained the same for the past few years? What about the performance of our NICU staff members (Medical and Nursing ) ? Are they improving themselves? That was the easy part. Now the difficult part. We can only improve a thing which can be measured. So to improve our NICU, we have to monitor some parameters of our NICU and then trend it and then find what we want to improve in that measure and then plan an intervention and then implement that intervention and then monitor the performance after the implementation of the interventions. (phew that was difficult to type right !) So lets see....if we heard that NICU in XYZ hospital had mortality of ELBW babies 5 years back of 50 % and that now they are reporting ELBW mortality of 20%...we definitely know they have improved themselves. How about nosocomial infection rate in a NICU in XYZ hospital was 5 per 1000 patient-days 5 years back and now was 1.5 per 1000 patient-days...we definitely know they have improved. One very nice example to illustrate this improvement is here: http://www.lafayettegeneral.com/pavilion/Level-III-Neonatal-Intensive-Care-Unit-1/Key-Performance-Indicators-3 There are so many parameters to be monitored in a NICU..I think we just have to select what is suitable in our setup balancing our resources. We have to be cautious not to overdo it...as then it will only be on paper and have no actual benefit for the NICU. the other (more difficult part) is to monitor the performance of NICU staff. Here also there are many options. One beloved one is compliance with infection control practices (especially ...hand hygiene). Success rate of intubations could be used for residents. How about IV infiltration (IV burns) rate for nurses? Morbidity/Mortality outcomes for consultants/attending ? Once staff know that they are being monitored...performance automatically improves. Once you start rewarding good performance......then people start having a healthy competition to improve themselves....the ultimate winner is the patient...NICU performance measures improve.....And thats the ultimate aim...to improve patient outcomes... The floor is open.
    2 points
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