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Apologies, I thought that the link will work. I upload the statement Cheers Statement on the application of NLS vs PLS Guidelines Oct 2023 V2.1_2.pdf

The UK resuscitation council issued a useful statement but I don’t believe it adequately addresses the needs of the population we’re discussing: ex-prem, sever BPD & CGA > 44 weeks.

Hi, We used the following for infants typically CGA at or after 44 weeks gestation who still require CPAP support. Most are recovering from a CLD

Hi, Sometimes steroids are used in this situation, but I tend to be cautious about it. Most of the evidence for postnatal steroids comes from studies in very preterm infants who remain mechanically ventilated, where steroids can improve lung mechanics and facilitate extubation. The DART trial, for example, was specifically designed to help chronically ventilated infants achieve extubation. It did not study infants who are already extubated and on non-invasive support, so applying that evidence to babies at 36–40 weeks CGA on CPAP is largely an extrapolation. For infants with established BPD who are already extubated, the evidence that systemic steroids meaningfully change the overall trajectory of the disease is quite limited. In my experience they may produce some transient improvement in respiratory mechanics, but the effect is often short-lived and oxygen requirements may increase again afterwards. Given the potential side effects, I am not convinced they provide sustained benefit in this group. in babies who are already extubated and on CPAP at ≥36 weeks CGA, I am not aware of strong evidence that systemic steroids significantly alter outcomes, and therefore I tend to use them very cautiously.

I think it would be helpful to first reach a shared understanding of the primary outcome we’re aiming for. In the case of babies at 22–24 weeks, I imagine survival is the initial focus, before considerations such as neurodevelopment and BPD become more prominent. With regard to HFOV, adjusting the frequency (Hz) typically affects the tidal volume delivered. If VG is enabled, increasing the frequency—perhaps to reduce CO₂ clearance—might not have the intended effect, as the ventilator will compensate by increasing the amplitude to maintain the set tidal volume, up to the user-defined limit, and vice versa. Cheers!

Hi, There are several factors that influence the ventilation strategy we pursue, and it often differs from baby to baby. DCC is important and, in my view, crucial. For babies born at <25 weeks, we typically proceed with intubation after birth, ideally in the NICU rather than the delivery room, and administer early surfactant. We prefer using the Dräger ventilator over other machines, as it’s dependable and allows for precise control. We use PC-AC with VG, targeting tidal volumes of 5–6 mL/kg, with a short inspiratory time and optimum PEEP. We don’t usually attempt extubation until at least day 3 of life, provided the clinical condition allows. Our philosophy is to let the baby “grow out of the tidal volume” rather than wean it too early. We also consider prophylactic hydrocortisone, particularly in the context of extremely preterm birth and early ventilator dependence. Routine sedation is generally avoided, as it’s often associated with the need for inotropes and increased risk of intraventricular haemorrhage (IVH). Caffeine is given as early as possible, ideally within the first 30 minutes of life. We also prioritise initiating mother’s own milk within the first 6 hours, even if in small trophic volumes. That said, this approach is different from the one we take in babies with evolving or established BPD, where the ventilation strategy changes significantly—and that’s probably a discussion for another time. Best regards,

This is my personal approach: If a baby remains on invasive ventilation with a hsPDA, and high peak inspiratory pressures (PIPs) are required to achieve adequate tidal volumes despite relatively low oxygen requirements (FiO₂ <40%), I tend to initiate treatment for the duct. I also generally opt to close the PDA before starting systemic steroids, particularly if there are signs of feeding intolerance or if steroid therapy is being considered for evolving BPD. However, I remain conflicted regarding the role of prophylactic PDA closure, particularly in a specific subset of extremely preterm infants—those born at <26 weeks’ gestation and weighing <500 grams. This group appears particularly vulnerable to pulmonary haemorrhage within the first 72 hours of life. I have witnessed several such infants deteriorate rapidly, ventilated or not, following pulmonary haemorrhage and, unfortunately, some do not survive. This experience continues to shape my cautious stance on routine early treatment in this population.

Hi there, I’ve worked in a few centres, and in Europe, Curosurf is the dominant product. However, in Canada, they use Bles, which is a bovine-based product. The dosage is 5ml/kg, which is a significant volume compared to Curosurf. This can sometimes lead to lung flooding and prolonged desaturation.

Thank you for sharing your thoughts and the helpful references! You raise a really good point—while aiming to normalise albumin may not always be necessary, there probably is a threshold where we’d start feeling uneasy, even in the absence of significant oedema. The tricky part, as you pointed out, is defining that threshold and understanding how low we can let albumin levels go before it starts affecting other physiological functions beyond oncotic pressure, especially in neonates. The UpToDate recommendation to maintain albumin levels above 2 to 2.5 g/dL is certainly a reasonable guideline. However, it’s intriguing to consider whether we should apply this universally or modify it based on individual circumstances, such as the severity of lymphatic loss or nutritional deficiencies. Additionally, did UpToDate mention anything about the use of Pre-albumin as a more accurate measure of nutritional status (I believe its half-life is three days)? I’ve attached a review of the general use of albumin. The authors believe it’s a practical point to administer albumin in chylothorax. However, they also point out that recent protocols don’t mention albumin and instead focus on fluid replacement, MCT diet, TPN, and octreotide. Thanks again for contributing to this discussion—this is turning into a great learning exchange! 😊 Shalish et al. - 2017 - Uses and misuses of albumin during resuscitation a.pdf

Hi Uvbogden, Thanks for your detailed message. I completely agree with your approach regarding the replacement of immunoglobulins and clotting factors. Replacing clotting factors during procedures or active bleeding makes sense, given their direct impact on clinical outcomes. However, I am sceptic when it comes to albumin replacement. The key question is: what is the clinical goal of replacing albumin? If the primary aim is simply to correct the numbers, it becomes problematic, especially when considering the difficulty in keeping albumin within the vascular compartment due to capillary leak, which can lead to fluid shifts and potential complications. Moreover, the half-life of albumin is about three weeks, meaning that serum albumin levels don’t accurately reflect the current nutritional state, making it a poor indicator of real-time nutritional adequacy. Relying on frequent albumin infusions just to maintain levels within a “normal” range could result in unnecessary interventions without a clear evidence-based benefit. From what I’ve seen, there’s limited evidence supporting routine albumin replacement in cases like chylothorax unless there’s a specific clinical indication, such as severe hypoalbuminemia contributing to oedema or fluid imbalance that cannot be corrected by other means. Most reviews focus on nutritional management (MCT-rich feeds, low-fat diet)and, if unresolved, escalation to TPN, octreotide, and potentially surgical options like thoracic duct ligation. I haven’t come across strong evidence advocating for regular albumin infusions as part of routine management. Curious to hear what others are doing in similar cases Best regards,

Hi NHowold, Thank you for your response. We typically use Monogen (MCT-rich milk), and I appreciate the tip on how to remove fat from breast milk. I’m curious about your practice regarding albumin—if albumin levels are below the normal range, do you administer intravenous albumin? I am looking forward to hearing your thoughts. Best regards,

Question to the group: How do you approach the management of chylothorax in your unit, particularly with regard to fluid replacement, nutritional support, and the use of albumin? It would be helpful to learn about your protocols and hear your experiences in managing similar cases. Your contributions could really help foster a more evidence-based discussion on best practices! For example, do you use albumin to increase oncotic pressure, aiming to draw fluid out of the extracellular compartment? Or do you administer albumin in cases of hypoalbuminaemia to support overall nutritional status? Alternatively, do you believe that albumin has little to no role in chylothorax management, and that the focus should primarily be on enteral diets(Monogen), total parenteral nutrition (TPN), and fluid balance? I am looking forward to hearing your thoughts and practices!

I’m not certain if evidence-based practice plays a role in this, but I believe it’s related to logistics. Most of the NICU staff will be trained in NLS/NRP, and I imagine that not many require training in APLS/PALS. However, there are other factors to consider, such as equipment (like a cuffed ETT) and drug dosages. In places where the NICU is part of a hospital that also includes pediatric services, if a child collapses, they call the pediatric crash team.