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#168 - 🔵 Managing Respiratory Distress Series - Episode 1 with Dr. Richard Polin

Hello Friends,

As the end of the calendar year is quickly approaching, we are happy to bring you a new mini-series focusing on the management of respiratory distress in neonates. We have a star-studded lineup of guests ready for you and we are kicking things off with a conversation with Dr. Richard Polin. Dr. Polin, the William T. Speck Professor of Pediatrics at Columbia University and a celebrated figure with numerous accolades including the Apgar Award, shares his profound insights on neonatal respiratory care. This episode primarily focuses on the critical aspects of managing respiratory distress in neonates. We delve deep into the nuances of respiratory support, discussing the crucial differences and impacts of flow and pressure. Dr. Polin's expertise illuminates the conversation, offering a blend of theoretical knowledge and practical experience. The episode covers various topics, including innovative treatment methodologies, patient care strategies, and the evolution of neonatal care over the years.

Our heartfelt thanks to Fisher & Paykel for sponsoring this series.


Watch the video below to learn more about how interface design can affect your therapy outcomes, or for further insight into the evidence, download the NIV in NICU Clinical Evidence Summary Booklet.

Fisher & Paykel Healthcare offer a full neonatal care continuum which helps provide the best start possible to our precious babies worldwide.

To help demonstrate the importance of interface, Fisher & Paykel Healthcare have created a neonatal airway simulator (Baby LIV) which is based off a 28–30-week gestational age neonate. The simulator helps visualize pressure and flow therapies. For more information and to book an in-person demonstration, go to


Short Bio: Dr. Richard A. Polin is the William T. Speck Professor of Pediatrics at Columbia University, College of Physicians and Surgeons and is the immediate past Director of the Division of Neonatology at Morgan Stanley Children’s Hospital of New York-Presbyterian. From July, 1977 until January 1998, Dr. Polin was a faculty member in the Division of Neonatology at the Children’s Hospital of Philadelphia and Professor of Pediatrics at the University of Pennsylvania. In 1998, Dr. Polin returned to Morgan Stanley Children’s Hospital of NY- Presbyterian as the Director of Neonatology. In the spring of 2006 Dr. Polin received the National Neonatal Education Award from the AAP’s Section on Perinatal Pediatrics and in 2017 he was inducted into the “Legends Hall of Fame”. Dr. Polin is the 2021 recipient of the Apgar Award from the American Academy of Pediatrics. Dr. Polin has published over 200 original papers, 20 books (including Fetal and Neonatal Physiology, Workbook in Practical Neonatology, Pediatric Secrets and Fetal and Neonatal Secrets,) and more than 200 abstracts. Dr. Polin is the Chair of the NICHD Neonatal Research Network executive steering committee, and he is the past chair of the Sub-board of Neonatal-Perinatal Medicine


Some of the articles mentioned by Dr Polin in this episode can be found below:

Gyamfi-Bannerman C, Thom EA, Blackwell SC, Tita AT, Reddy UM, Saade GR, Rouse DJ, McKenna DS, Clark EA, Thorp JM Jr, Chien EK, Peaceman AM, Gibbs RS, Swamy GK, Norton ME, Casey BM, Caritis SN, Tolosa JE, Sorokin Y, VanDorsten JP, Jain L; NICHD Maternal–Fetal Medicine Units Network.N Engl J Med. 2016 Apr 7;374(14):1311-20. doi: 10.1056/NEJMoa1516783. Epub 2016 Feb 4.PMID: 26842679 Free PMC article. Clinical Trial.

Dargaville PA, Kamlin COF, Orsini F, Wang X, De Paoli AG, Kanmaz Kutman HG, Cetinkaya M, Kornhauser-Cerar L, Derrick M, Özkan H, Hulzebos CV, Schmölzer GM, Aiyappan A, Lemyre B, Kuo S, Rajadurai VS, O'Shea J, Biniwale M, Ramanathan R, Kushnir A, Bader D, Thomas MR, Chakraborty M, Buksh MJ, Bhatia R, Sullivan CL, Shinwell ES, Dyson A, Barker DP, Kugelman A, Donovan TJ, Tauscher MK, Murthy V, Ali SKM, Yossuck P, Clark HW, Soll RF, Carlin JB, Davis PG; OPTIMIST-A Trial Investigators.JAMA. 2021 Dec 28;326(24):2478-2487. doi: 10.1001/jama.2021.21892.PMID: 34902013 Free PMC article. Clinical Trial.

SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network; Carlo WA, Finer NN, Walsh MC, Rich W, Gantz MG, Laptook AR, Yoder BA, Faix RG, Das A, Poole WK, Schibler K, Newman NS, Ambalavanan N, Frantz ID 3rd, Piazza AJ, Sánchez PJ, Morris BH, Laroia N, Phelps DL, Poindexter BB, Cotten CM, Van Meurs KP, Duara S, Narendran V, Sood BG, O'Shea TM, Bell EF, Ehrenkranz RA, Watterberg KL, Higgins RD.N Engl J Med. 2010 May 27;362(21):1959-69. doi: 10.1056/NEJMoa0911781. Epub 2010 May 16.PMID: 20472937 Free PMC article. Clinical Trial.

Morley CJ, Davis PG, Doyle LW, Brion LP, Hascoet JM, Carlin JB; COIN Trial Investigators.N Engl J Med. 2008 Feb 14;358(7):700-8. doi: 10.1056/NEJMoa072788.PMID: 18272893 Free article. Clinical Trial.

Morowitz MJ, Katheria AC, Polin RA, Pace E, Huang DT, Chang CH, Yabes JG.Trials. 2022 May 23;23(1):428. doi: 10.1186/s13063-022-06352-3.PMID: 35606829 Free PMC article. Clinical Trial.


The transcript for today's episode can be found below 👇:

Ben: 0:00

Hello everybody, welcome back to the Incubator podcast. We are back this Monday with a special episode looking at a topic in neonatology that we are all dealing with, which involves managing respiratory distress in neonates, and we're focusing on aspects of flow versus pressure in how we deliver support to neonates. So we're very excited to be joined by a former incubator guest, one of the giants of neonatology, dr Richard Pollin. Dr Pollin, thank you so much for making the time to be on with us today. It's my pleasure. Daphna, how are you? I skipped you Sorry.

Daphna: 0:36

That's okay. It's always such an honor to have neonatology grapes like Dr Pollin in the studio, so I know we're both starstruck yeah it's always fun.

Ben: 0:49

I mean, when the opportunity presented itself, we definitely did not shy away from it. We jumped on it and we're very excited to be talking to you about this. Dr Pollin, I think the first place I would like to start is really having a broad overview of what we are actually dealing with, and what I mean by that is that, when you are faced with a baby that is in respiratory distress, can you give us, like, what your differential looks like and what are the things you're thinking of in terms of what could be going on with this patient?

Rich Polin: 1:22

Sure, the most common reason we see for respiratory distress simply has to do with slow transitional physiology. As you know, baby start with a fluid filled lung with lower pulmonary blood flow and less systemic blood flow. During the transition the placenta is removed, cardiac output increases and pulmonary blood flow increases. But during that time it is very common to see babies with some degree of respiratory distress, hypoxemia, retractions. That gradually disappears and I usually consider that to be slow transitional physiology. If it's due to pathology, there are a variety of causes, from something quite simple such as transducer to kidney to the newborn, which is delayed reabsorption of lung fluid or respiratory distress syndrome, a chronic aspiration, malformations in the lung or cardiac. causes of respiratory distress, congenital heart malformations those are probably the most common causes, pathologies that we encounter in the NICU.

Ben: 2:32

That's interesting, and so the reason I'm asking that question is because some people may think what's even the point of entertaining a differential, because it feels like these babies are treated pretty much always the same way, no matter like it seems like all these kids, especially when they're born and they're full term, it's like, well, just start on some bubble CPAP and call it a day. Is there a blanket approach to the management of respiratory distress in the neonate, or does your differential influence how you will take care of these babies?

Rich Polin: 3:01

So yes and no. So the immediate response to baby respiratory distress, besides making sure that vital signs are okay and their oxygenation is okay through pulse oximetry, is to provide some minimal level respiratory support. That usually involves CPAP. At Columbia we use bubble CPAP, but there are other ways of providing CPAP. Some centers might use high flow nasal cannula as an alternative. So it's stabilization. And then, once the baby stabilize, you go through your differential diagnosis and decide whether further interventions are necessary, depending on what disease process you think is going on. Obviously, if it's cardiac disease, you're going to probably end up getting an echocardiogram to evaluate for cardiac malformations. If it's suspected pulmonary disease, you're going to be getting a chest x-ray and then making your next step in care. Depending on what you think the primary disease process is going, it's happening.

Daphna: 4:04

I think that's a great approach. We talked a lot on the podcast about the baby's pertinent past medical history, which really is just when they were a fetus as a dyad. I wonder what aspects of the maternal history delivery factors that give you a better understanding of what respiratory pathologies at play.

Rich Polin: 4:29

That's a great question. History is critically important. If you're suspecting infection, you want to look for historical features in the mother or sisterly, suggestive of infections such as preterm premature membranes, prolonged rupture membranes, signs and symptoms of chorioamnionitis as defined by the American College of Obstetrics and Gynecology. Was there a meconium in the amniotic fluid which makes the diagnosis of a meconium aspiration syndrome more common? Is it a preterm delivery or a very preterm delivery, where respiratory distress syndrome might be the most common pathology that we encounter? Or is it a late preterm delivery, for example a baby delivered by an accessory infection, where a transient to give you the little more might be more common? Again, was there normal amounts of amniotic fluid, decreased amounts of amniotic fluid, which might suggest pulmonary hyperplasia, or excess amniotic fluid might suggest a GI malformation of the baby?

Ben: 5:34

I am wondering, dr Polin, with your experience, what are some of the big turns that we've taken as a field in how we manage respiratory distress in the NICU and how have these different steps in how we've changed how we approach this disease? What do they tell us about our understanding of the different pathologies? Knowing your vast experience, I'm just curious when you're looking back at how we treat this today and how we treat this when earlier in your career, what is your perspective on how far we've come?

Rich Polin: 6:05

So you say earlier in my career. That really means in the 1970s and in the 1970s. That was the beginning of CPAP use. When I went from Columbia to Children's Hospital of Philadelphia, they weren't using any CPAP at that time and babies with severe distress were just intubated and ventilated. It was the pre-surfactant era and that was ventilating. A baby who has RDS without surfactant is a recipe for creating a baby with chronic lung disease or bronchopulmonary dysplasia. Surfactants were developed in the 1980s and revolutionized the care of pre-term babies with respiratory distress syndrome and decreased mortality from respiratory distress syndrome. At that time we had concurrent increase in the use of antenatal steroids which decreased the frequency and severity of RDS, also decreased mortality and interventional hemorrhage. So a variety of things happened. But first thought, before ventilating babies for a long period of time, was to give surfactant. And the next iteration I think came from the randomized secret trial was comparing non-invasive ventilation, which again had its origins in the 1970s, with standard ways of intubation and surfactant, showing that the outcome that outcome being death or chronic lung disease was less in babies who were treated with non-invasive ventilation rather than intubation and surfactant and then ventilation. The final iteration, which is still being studied, is the use of different ways of giving surfactant instead of intubation, giving it through something called LISA, which is less invasive surfactant administration. So we moved away from just ventilating without surfactant to ventilating with surfactant, to first considering non-invasive ventilation and then refining which. If we have to give surfactant, what's the best way to give it. So that's what's happened in RDS and in the other severe disease which is meconium aspiration syndrome. We've moved away from the 1970s, from intubating and suctioning every baby born through meconium, to selectively intubating babies who appear to have difficulty with ventilation, but not doing routine suctioning of the airway of babies born through meconium. So that's a big change. Perhaps in the last 10 years that's revolutionized what we're doing.

Daphna: 8:46

I appreciate the historical context and we've got so many challenges of modern medicine, but I cannot imagine working in the ICU before the days of CPAP and surfactant. It certainly was a different time.

Rich Polin: 9:01

Yeah, a very different time, and mortality was much higher. The outcomes were not as good. Babies were sicker, ventilated for longer periods of time and many ended up with chronic lung disease.

Daphna: 9:14

And you've alluded to this a little bit, especially how we have changed the trajectory of RDS because of surfactant. But maybe you can talk a little bit about how kind of the path of physiology itself of RDS has kind of changed over the years, especially as we are bringing in a younger and more immature population.

Rich Polin: 9:38

If we go down to babies at 22, 23, 24 weeks of gestation, they have alveolar ducts, they may have alveolar sacs but they do not have true alveoli. And at that time surfactant production is just beginning. And if you lack surfactant, if you maybe lack surfactant lying on the alveolus and end the expiration, this tendency is to collapse those structures and that's what causes the reticulate granule appearance we see on chest x-ray in babies with RDS. The presence of surfactant decreases surface tension and allows those structures to remain in patent, but true velar development is not completed to about 35 to 36 weeks of station. So our very immature babies are working with alveolar ducts, alveloar sacs, but not true alveoli and probably insufficient not zero amounts of surfactant but insufficient amounts of surfactant. And in addition to surfactant there's other structural abnormalities in the longer preterm babies which makes it harder for them to continue to deal with respiratory distress.

Ben: 10:50

Now we're getting into really the management of RDS. I wanted to ask you about how important is it for clinicians to realize that management has to be done right. I feel like you were describing how, in the early days of your career, one of the outcomes that you were facing was mortality, and that's something that is quite striking to me because we since, during my training, the expectation was that a baby, especially a falter, maybe an RDS, was not expected, is not expected, to die by no means, and so it feels like we've discussed some of these different modalities. We've talked about CPAP, we've talked about intubation, we've talked about surfactant and we've talked about all forms of nasal cannula. But, in your opinion, why is it important to think critically about these babies and about the interventions that we are using, in light of what maybe morbidities are at play and why that matters for these babies and their families?

Rich Polin: 11:47

Sure, every intervention in the NICU has a cost, a risk of side effects, I think in my latest podcast, I think, I said don't just do something, stand there, and before you start to do something that's invasive in newborn, you have to ask yourself is the therapy that I'm applying going to have a benefit, or does the risk of a complication outweigh any benefit from what I'm doing? For example, ventilation. Ventilation is literally even short-term ventilation. CPAP has the ability to injure the lung and set up an inflammatory response which ultimately results in chronic lung disease. So ventilation carries with it a risk for a baby. Surfactant carries with the risk You're giving a liquid down in the lung and whether you're giving that surfactant through lisa or through intubation and pouring it down through the endotracheal tube. Those are pretty stressful procedures for a newborn baby. I know we should try to do it as gently as possible but, for example, in babies who are getting suffocated, people have demonstrated that the EEG becomes flatter or flat during that process and I think that even with lisa it's a stressful procedure. You're using a laryngoscope to cause significant cardiopulmonary compromise for the baby, and noninvasive ventilation is not without complications. Although we generally don't see air leak or pneumothoracies with something like CPAP. They do occur and, depending on the kind of CPAP you're using, there's a risk of nasal irritation or nasal septal compromise. So every therapy that we're using in the newborn baby has a risk of complications, and that's why I go back and try to say before you think about doing something which is invasive, even something as simple as CPAP, ask yourself what is the benefit for the baby. Am I going to? Am I dealing with the pathophysiology of the disease that I'm encountering?

Ben: 13:57

That's such an interesting point because I think that as neonatologists, right now we are asked to work really hard. We're covering more and more babies and we have more and more administrative tasks and we often get these calls from the delivery, the labor and delivery suites, saying hey, there's this baby, he's having slight respiratory distress and really the reflex could be oh, just let's start some CPAP, let's bring this baby to the NICU as a solution, without sometimes considering all the things you just mentioned, which are what am I doing to this baby in terms of intervention? What are the potential complications? I am wondering, in your opinion, since we started this discussion talking about transitioning and how respiratory distress could be an issue of slow transitioning, what is, in your experience, a good cutoff to say, all right, I'm going to watch this baby because maybe that's just transitional. And I've seen people say I'm going to wait 15 minutes, some people wait a few hours and I'm just curious, in your experience, what is the right time to say, okay, this is no longer something that can be just watched and that just needs now some form of intervention?

Rich Polin: 15:06

So I guess I have two answers for that question. One is there's absolutely no number that I can give you that says this baby should be over its transition, but for me four to six hours seems to be a reasonable time to say is the baby's respiratory distress improving? Is the baby looking more active, if I'm thinking about infection? So for me I wait four to six hours before embarking on a more invasive therapy for that baby or perhaps starting antibiotics for that baby, and during that time the baby should be getting better. So in other words, if the Fio2 is 30% and then two hours later is 50%, that's a baby who I'm going to intervene, much sooner than if a baby is in 40 or 50% and then two hours later it's in 30%. And if the respiratory distress seems to be getting better During that time, it's okay to use something as simple as CPAP, which we commonly do during that transition, but usually nothing more invasive, because we're just expecting the baby to make its transition and many babies end up with 21% oxygen. So overall, four to six hours seems to be a reasonable time to watch the baby before embarking on something different.

Daphna: 16:25

I think that speaks to your expertise and obviously your experience really about the art of medicine. It's simpler to just bring the baby over, put them on CPAP, start IV fluids and antibiotics. It's much more work for the clinician, I think, to sit at the bedside and be patient and not intervene, even though it might be the right thing for the baby. And I'm wondering if you can share kind of some of those lessons from your career about waiting and being successful, waiting and not being successful or having intervened and then feeling like gosh. I really didn't need to do all of that.

Rich Polin: 17:11

So you say something really important, and that is sitting at the bedside. Clinicians can't look at a baby and say, all right, let's wait for the transition to occur and walk away. Good clinicians have to be at the bedside and watch the baby's signs and symptoms. Are they improving? Are the retractions becoming less? Is the FIO2, inspired Reaction Constriction improving? But you have to be at the bedside or within a few feet of the bedside to decide what's happening with the baby. You can't do that by intermittently walking back and forward.

Ben: 17:48

You're preaching to the choir here. Daphna is a hoverer. She loves to hover around the bedside.

Daphna: 17:56

To my nurses' dismay. They want me to leave the bedside and I just that's not how I doctor.

Rich Polin: 18:03

Don't leave the bedside, watch the baby closely, and I think that's how you practice good medicine is by watching the baby, watching the baby breathe, even under a CPAP. One of the common mistakes I see in my own NICU is a fellow who said, oh, I put the baby on a CPAP and the FIO2 is 40% and the saturations are approaching 90%. I said, oh, baby must be doing great. And then I put my stethoscope on the baby's chest and I said these babies are not moving in the air, not ventilating. So the appreciation of ventilation, especially pre-temperature, is RDS, I think is a law of thought and I say get a gas or let's do something different to improve ventilation. But physical examination and careful observation are the keys in babies making that transition and knowing when to intervene with more invasive therapies.

Ben: 19:10

Since we've talked about this question of respiratory distress, I think what's interesting to me right now is that neonatology always felt like we were dealing with the population of babies and it was one and the same, and we may have said, okay, we have our full terms and we have our preterms, but I think now the care of neonates is segmented so strikingly between the different gestational age groups. We have the postterms, we have the term babies, we have the late preterms, we have the preterms and then the extremely low birth weight infants I am just curious about I want to start to maybe go one at a time the late preterm infants are the ones, in my opinion, that are the most challenging, especially when it comes to respiratory distress, because, as you said, we're not exactly sure what is supposedly expected versus just pathological, and so I'm wondering if you have any advice as to how should we look at a baby that is born with some degree of respiratory distress at these late preterm gestation, like 34 weeks and so on.

Rich Polin: 20:19

So I think here physical examination is key. Is it a baby who is breathing at 80 or 100 times per minute? May not be grunted or maybe have intermittent grunting, has retractions and when you measure blood gases they have some degree of hypocarbia. They're ventilating well but may have an oxygen need and the chest x-ray has signs compatible with transient kidney of the newborn. Those babies do well In TTN. The misnomer is the first city is transient. Of course some of those babies can be able for days, three, four days, and some of those babies require high oxygen concentrations. Fortunately, I think, many obstetricians are now giving antenatal steroids to babies who are considered late preterm, based on the Alps trial which showed a decrease in mention to the NICU for respiratory distress, and so many of our babies have milder disease and those steroids, I think, help to activate the sodium channels in the lung and help to remove lung water so that the diseases we're seeing are relatively mild, so that disease is usually just treated non-invasively with some form of noninvasive ventilation.

Ben: 21:39

In terms of treatment of babies with RDS. One of aspects of the treatment involves rolling out pneumonia and other forms of infection, and the question that always comes up is well, could a baby born preterm not be in respiratory distress, and when do we interpret respiratory distress as a form of illness that may have infectious origins, versus saying no, this is just a physiologic response to being born early? I know this is there may not be a correct answer, but I'm just curious as to when do you, as a clinician and with your experience, draw the line and say well, this is what I accept for a baby born preterm, In terms of them having some difficulty breathing, versus? This needs to be covered from other standpoints, like an infectious workup, antibiotics and so on.

Rich Polin: 22:31

So that's a great question. So we've already talked about historic information which could suggest infection, chorioamnionitis, using the current ACOG criteria, not just fever in the mother and pulmonary rupture membranes and preterm, premature rupture membranes. And then we get a baby. If it's a critically ill baby, meaning that it's a baby you had to intubate and ventilate right from the word go with severe respiratory distress syndrome, I think all those babies get treated with antibiotics because there's so will and you never want to miss a baby, even when they're not maternal risk factors for infection. You don't want to miss a possible infectious complication. That's a small subgroup there's most of the babies have other veering, less severe respiratory distress syndrome. And if there are no risk factors for infection in those babies, I think the, for example, the babies born by elective caesarian section for maternal indications, I think the committee of fetus and newborn criteria would say don't treat with antibiotics, just observe those babies. If there are some risk factors for infection other than chorioamnionitis, it's unclear whether you should treat babies antibiotics. And just to put a plug in for an ongoing trial, there's the nano trial, nicu antibiotics and outcome trial, which is randomizing babies whose mothers do not have chorioamnionitis. They stop, born by elective caesarian section to receive antibiotics or placebo. So we don't have an answer to that question, but I think that in the majority of babies, it's very safe to wait before administering antibiotics, the one exception being if the mother has chorioamnionitis. You should not wait, get a blood culture and start the baby on broad spectrum antibiotics.

Daphna: 24:31

I think that's very helpful. In particular, I agree with Ben, those late preterms where we say well, or even the moderate preterm infant we say could this be premature or could it be something else? We'd love to get your opinion on, obviously, the changing landscape with the extremely low birth weight infant, there's a lot of debate in the community about which babies need intubation right away, which babies can we wait on, which babies are too small or too unstable for Lisa and need to be intubated, or which can we manage noninvasively, sometimes even without surfactant, especially after the administration of anti-natal steroids and some of the other fetal stressors that mature the lungs. So I'd love to hear your thoughts about the management of those tiny babies.

Rich Polin: 25:24

So I guess you're talking about babies 22 through 24 reach the station and the new number in all of that is the baby 22 weeks at the station. We all know the Iowa approach which is very protocolized about ventilation of those babies. I don't think we know the right way to approach those babies with ventilation. In my NICU we would always try noninvasive ventilation first. If the baby is breathing spontaneously and in that range of 22 through 24 reach the station, babies would do well about 30% of the time using noninvasive ventilation. About a third need intubation immediately because they're sick and about a third will eventually decompensate. We do not use NIPPV routinely in babies RDS. We use it post-extubation but not use it as a therapy and pre intubation NIPPV sending noninvasive positive pressure ventilation. So we would always try noninvasive ventilation For those babies that do need ventilation. I don't know if we need or I don't know if we know the right way to ventilate those babies. The one which is most appealing to me is high frequency oscillatory ventilation. I've heard in Tom Viac-Trom say that high frequency oscillatory ventilation is CPAP with the wiggle.

Daphna: 26:55

I like that thought.

Rich Polin: 26:59

I think using high-frequency oscillatory ventilation maybe I put the word in quotes maybe the right way to treat those very tiny babies who need non-invasive ventilation. We don't know, but he has great success in his unit in the Netherlands managing babies in that fashion.

Daphna: 27:19

I love, actually, your ability to say we don't know. I feel like so many in the community are staying like this is the right way to do it and the other part of the community is saying this is the right way to do it. Again, given your career and how many times we've been right but also been wrong in the management of babies, what do you think is the best approach?

Rich Polin: 27:47

while we're still trying to figure it out in having those conversations, Again, think of what you're doing, what's least likely to cause morbidity or mortality in the baby. I'll give you an example of a mistake that we did earlier in my career in babies with pulmonary hypertension, for example, meconium aspiration, pulmonary hypertension we used to hyperventilate those babies and drive their CO2 down to 20 or 18 or even lower, and that was a work she did with pulmonary hypertension many times but left the baby with serious lung injury and made those babies ended up hearing loss. So that was a mistake. We did Rose at Shop for many years until we realized that was not the right approach for babies with PPHM. So I think you decide on a therapy by looking at the baby and thinking about the baby's underlying lung disease and it was just a very immature baby with respiratory distress syndrome. Use the least toxic therapy you can get away with and for me, starting with non-invasive ventilation CPAP is what we use at Columbia and then, if a baby does require ventilation, think about using the lowest pressures you can to ventilate that baby. And again, I like the idea of high-frequency oscillatory ventilation the very tiniest babies, which is what we tend to do at Columbia.

Ben: 29:16

I have to share a pet peeve of mine because, as we're talking about using non-invasive ventilation in some of our smaller babies, even as a trial, I have this fear that I will be the clinician who manage the baby. That's like 25 weeks, because I don't know if 22 weeks really matters in that scenario. But managers are like a 25-week-old non-invasive and this baby doesn't get surfactant in the first day or so. And I know that I can get, probably, according to the evidence, the most quote-unquote bank for my buck with surfactant in the early phase of respiratory distress. And so I'm worried that I'm like are we going to be the unit that has not offered the potential for surfactant therapy to a 25-week-old? Because we were arduously trying to maintain this baby on non-invasive, and I feel like the evidence tells me that this is unfounded. But I'm just curious how do you feel about that? Like, are we really going to try to keep this baby on non-invasive? Because it's even the ones who do OK, it's never really a pleasant, smooth ride. It's always. You're always worried. Oh my god, are they failing non-invasive? Are they failing non-invasive? That's always the question. And so how do you negotiate that, where you are having the surfactant always looming in the background and saying oh man, should I just put down the tube and give that?

Daphna: 30:32

Yeah. Or we have kind of those middle of the road babies where they stay kind of prolonged on respiratory support and you're like, but they didn't get surfactant.

Ben: 30:41

Maybe if they'd gotten surfactant would we be farther in the course, and then the parents come back to you maybe two weeks later and they said why hasn't my baby gotten this surfactant that every other preterm kid supposedly gets? And you're like, oh boy, how am I going to explain that?

Rich Polin: 30:54

Both are great questions. The fact is that I'm in therapy. When we looked at trying to predict which baby we need intubation and surfactant a number of years ago and the same was done by the group in Melbourne it was very hard or nearly impossible to predict which babies would fail non-invasive ventilation. Clearly babies who have severe white-out on x-ray and are needing a high concentration of oxygen. Those babies need some sort of intervention. At Columbia we tend to choose a cutoff, fio to 60%. So if a baby is increasing, getting worse and we reach that threshold of 60% or the pH is less than 7.2 with pH greater than 65, we tend to intervene with another therapy at that point. But other centers use lower thresholds for intervention. I think it's worth looking at the Optimist. A trial gone in Melbourne published in the list two years ago In JAMA. It would say you intervene giving surfactant through mist or ELISA when babies run 30% oxygen, showing not a significant benefit for death or chronic lung disease, but individually chronic lung disease was less and need for ventilation was less in babies who had that intervention at 30% oxygen. I don't think we know when to intervene with surfactant in a baby. On non-invasive ventilation, I guess it depends on your skills at using non-invasive ventilation. Some of the issues have greater skills than others at keeping babies off conventional mechanical ventilation. But we have found that 60%, using a threshold of 60%, does not increase morbidity or mortality. But I understand the bind role in it. The baby ends up getting more severe lung disease, ventilated two weeks of life and the question is would the baby have done better with surfactant? Perhaps we just don't, I don't know. I don't think we know that answer, but it's worth looking at the Optimist trial.

Daphna: 33:03

I think you bring up another good point, though, about your unit's criteria, which again is different from other units in the country, but about having a standard protocol for a unit, like a threshold that everybody does an intervention. What are the benefits for having kind of this standardization across a unit?

Rich Polin: 33:27

I think it's a way of looking at outcomes and decreasing variability. So if you're in a unit, you're picking 40% as your threshold or 30%, which I think is low at oxygen concentration for our intervention. It gives you a way of looking at your outcomes in a standardized fashion. But if one clinician is using 30%, the next clinician is using 60%. It becomes problematic to say what is the best route for those babies. And, by the way, in the original trials comparing non-invasive ventilation to surfactant to an endotracheal tube, the SUPPORT trials use a lower threshold than the trial out of Australia, because that was the COIN trial out of Australia which used 60%. So I think that there's a lot of variability in the world, but decreasing the variability within a NICU I think is worthwhile in terms of looking at outcomes.

Ben: 34:24

Our last question for you today, Dr Polin and I think that would be a great segue to our next episode tomorrow is related to how clinicians need to understand what kind of therapy is actually being delivered at the bedside. I feel like, from a technological standpoint, there's a lot of ways now that we can deliver non-invasive ventilation, or CPAP, and I think that as clinicians, we are again so busy and we have such a nice team that we can often delegate that to our respiratory therapist and we say, oh, start CPAP. And it's not always the same whether you're delivering CPAP via a bubble interface, whether you're delivering it via a ventilator, what kind of interface you're using at the baby's face. Without going into the details, because we'll cover those how important is it for people to actually be competent in understanding the various differences in what they're doing? Because I have a feeling, based on what you've told us this far, doing the right thing early on can really impact the following steps when it comes to management and decision making for these babies.

Rich Polin: 35:38

I think you raise a critical issue, that all non-invasive ventilation is not identical. You have to think is it the right interface that's going to deliver CPAP effectively? Is it the right generator for the CPAP? Is it a bubble CPAP, where you create expiratory pressure using a fluid where the expiratory limb is put into a volume of fluid down to a certain number of centimeters? Is it a fluidic flip device, which supposedly has decreased resistance during expiration? Is it a ventilator? And there are different ways of applying CPAP. They all have physiological differences and before you choose one for example, ventilator CPAP versus bubble CPAP you're to think to yourself and say is this the right way to doing it for a baby? Am I getting the biggest bang for the bump? So I'm sure you're going to talk about that coming up, but there are significant differences demonstrated in babies, in in vitro models and in animal studies.

Ben: 36:44

Thank you very much, because I think this is really where we're hoping to take the discussion next as to how do we, how do we, excel at providing the most optimal treatment for these babies in order to reduce both mortality, morbidity and also the need for any additional therapy. So, thank you, thank you for mentioning that, and I think this will be a great segue for our next episode. Dr Polin, and thank you very much for making the time to be with us today. We look forward to chatting with you again tomorrow, definitely. Thank you for being here, as always, thank you, I am.

Rich Polin: 37:18

I was delighted.

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