bimalc

The issue is that in most resuscitation (at least in my experience) you cannot be confident which is the case at the moment that you are handed a grey and lifeless baby. You are forced to proceed with full resuscitation and if you need volume and O- blood is available, given the alternatives, it seems reasonable to push some blood (of course, if you need volume and appropriate blood isn't available push saline as Stefan suggested - in the acute phase if you're in that much trouble you probably just need some preload while you try to get the heart going again)

in VLBW who is not edematous we use BW until 14d or until regain of BW, which ever is first. In the case of an edematous baby, our local practice is not uniform and I think you really need to tailor that to the clinical course (continued edema, or had some diuresis and now is gaining weight again but this time it is 'good weight' and not 'water weight', etc.)

I'm not sure we did anything particularly involved, iNO at 20ppm and assess if responder or not based on FiO2 requirement (although, in practice, I feel like no one ever turned the iNO off in non-responders, the kids just died eventually). We would try to get ECHO for indirect estimation of PH before starting (and to make sure this wasn't anomalous veins). My original comment still stands though: as this patient sounds like they have evolving CLD, I'd invest more of my time and effort in reviewing XRays and optimizing the vent for CLD. Also, if you haven't started, I'd have a very frank discussion about morbidity and mortality with the family. Have you considered re-posting/cross-posting to the virtual NICU if you are interested in discussing a specific patient? Bimal

I agree with Nathan about it being very easy to forget about the 'other' sources of fluid the baby is getting and that these are more significant the smaller the baby gets. One thing I will take exception to is TKO fluids for the second lumen of UVC. I would argue that if you care about volume of infusions in a specific baby, you should be writing your orders such that you don't need a TKO in the second lumen (either by running needed things in each lumen or by using a splitter to run one back through both lumens). Furthermore, if your baby is small enough/sick enough you need to be counting the UAC fluid into your total. When we write for fluids out of the DR, our practice is to specify the total fluid goal inclusive of all infusions. If the baby is small enough or edematous enough, we will also ask the pharmacy to maximally concentrate all medications and give us their best estimate of all drug volumes and flushes etc. The challenge then, becomes picking a number to target. The second table you posted best approximates our local practice, with the understanding that we're including almost everything, not just nutritional fluids in this volume. For the sickest/smallest we're then following urine output and serum sodiums as a guide to whether or not we're over- or under-shooting on total volume. As regards BP targeting, we are VERY permissive of low MAPs if there is no evidence of impaired end organ perfusion, especially in the first 6-12 hours or even 24 hours. Over the period of 24-72 hours we start to care more about MAP > 30mmHg even in the absence of evidence of organ dysfunction. Finally, as regards your hypothetical patient, I would pick some dry weight, probably birthweight unless born edematous.

Current local practice is neither. I think the evidence from PREMILOC is compelling and would prefer to either make it our routine or at least have a conversation with parents about this very early on, but I do not think I will be able to convince my group to do this as I am not part of our 'BPD team' and local culture is to view BPD as an acceptable outcome as long as the patient is discharged off O2 or with a low flow cannula only (and our current practices are very effective at this).

We used it in crisis during my fellowship with the goal, obviously, of transitioning to some combination of sildenafil, trepostinil, bosentan etc. Was there a specific aspect of therapy you had questions on? My experience with using iNO in this circumstance is that many, if not most of the 'bad BPD' we saw, the clinical manifestations of pulmonary hypertension were more helped by aggressive respiratory support as opposed to pulmonary vasodilator therapy. We would get many patients as transfers from level IIIs to our BPD program at the level IV ICU and these babies would be been on non-invasive support for very long periods of time and, in retrospect they had been retaining CO2 and were on far too much FiO2. These babies ended up in pulmonary hypertensive crisis around transport and needed iNO for a period, but it wasn't the iNO that 'fixed' things, it was choosing an appropriate ventilatory strategy with things like much higher PEEP, including possible use of peep titration during bronchoscopy, transitioning to a higher tidal volume and lower rate strategy (very different strategies designed to prevent BPD and much more like what our colleagues in PICU are used to doing). Steve Atman gave an excellent talk on this point at PAS a couple of years ago and has published quite a bit in this area.

I've only rarely used that particular term/code and then in the context Stefan mentioned. If a patient is truly encephelopathic without obvious antecedent asphyxial event, though, I will code neonatal encephalopathy P91.819. My one comment if you're trying to learn about this patient population is that, at least where I did my fellowship, maternal SSRI exposure seemed to be significantly over-represented in this population and I can recall cooling several babies who in retrospect probably had SSRI exposure not hypoxic insult.

To be fair over ventilation/hypocapneia would be a very strong indication for extubation (the whole point of cooling is to save the brain, after all) however, in my experience this is exceedingly uncommon

Are you relying solely on leak compensation from your vent or are you using cuffed tubes to manage the leak itself?

Many thanks. Where do you set your PIP alarms? More generally, how concerned are you about peak pressures and 'barotrauma'?

What approaches are in use around the world for the ventilation of CDH (especially pre-operative on or off ECMO)? Many guidelines continue to list PIP limits based on earlier studies of 'gentle ventilation' improving survival, but these studies were done before significant advances in microprocessors enabled accurate volume targeted ventilation. Given what we know about the importance of volume-trauma as opposed to baro-trauma, is anyone volume ventilating pre-operative CDH and permitting higher peak pressures?

24-72 hours after cooling. I try to use spontaneous breathing modes in this setting whenever I can to try and get more information to guide counseling if I am concerned there will be an extubation failure. For example, the draeger VN500 has mandatory minute ventilation mode and has some lovely graphics that you can show a parent so they can see their child go apneic or hypopneic (CPAP/PS can be used to a similar but not identical end)

I must agree with the others that therapeutic hypothermia is not, in and of itself, an indication for intubation. However, given the known natural history of HIE, even in the era of cooling, I certainly have a lower threshold to intubate when the respiratory status is marginal. Also, must agree with @Stefan Johansson once the ET tube goes in, it does not come out (In our case, not until we get the MRI).

We also use the PINT cut-offs. However, I want to call people's attention to the problem is knowing what device you are using to measure H/H If your institution has POC or on-unit Hgb/hct available (for example on an I-stat or similar device or on a blood gas analyzer in the ICU) you need to ask your lab what the accuracy of those devices is compared to a formal H/H in the main lab, particularly at the low end of the Hgb range where you will be making transfusion decisions. The chemistry for some of the POC devices is influenced by what else is in the sample. For example the I-Stat (the POC device I am most familiar with) only calculates a Hct, not a Hgb (it just divides the Hct by 3 and reports that number as the Hgb). The Hct it 'measures' is corrected for Na (but not other electrolytes which may affect conductivity - the method by which Hct is calculated/measured), there is no correction for leukocytosis and the machine does not adjust for low TP or hyperlipidemia (but there are published manual corrections you can use). There is also the problem that these devices are validated for their correlation with a gold standard over either a normal range or a 'clinically relevant' range. Unfortunately, accuracy is really not relevant over most of that range. What we, in the ICU, care about is accuracy specifically down at the transfusion threshold. I don't really care if my pt's Hgb is 14 or 14.5 but I might care a great deal if it is 7 vs 7.5. To my knowledge, there is no such data for the I-Stat (nor any other POC device that I know)

I've used an LMA for the specific indication of 'can't ventilate, can't intubate' in somewhat larger neonates (not for surfactant); we do have size 0.5 available now (I've never used them). The only time I've used them in a DR setting was once when called emergently to a non-birthing hospital for premature triplets and I wasn't confident everyone could be intubated if BMV wasn't working. Even in that case we ended up not giving surfactant until back in NICU and intubated. The single biggest use case I've used an LMA for was palliative where patient is DNR/I and we're waiting for family to come in because of a decompensation and the patient REALLY needs PPV, we've placed an LMA and hooked it up to a vent until family can get in. My experience is that families (and frankly staff) perceive this as less invasive/harmful than intubating and then pulling the ET tube when parents are there. How was I trained? Sim sessions in residency and fellowship and at PAS the past few years it seems there has been an airway skills workshop that I try to attend it there isn't a conflict.

Does anyone have experience using a proximal flow sensor with an AVEA ventilator in Volume Guarantee mode? What is the smallest volume that can be reliably delivered?

I'm not sure whether the issue is equipment vs. us not really understanding what sorts of 'events' it is safe to have at home. The CHIMES study clearly shows that even well past term corrected many babies will have minor events that no one really ever notices because they aren't looking. There is reasonable evidence that you can ignore brief events without compromising safety (probably because many brief events reflect monitor limitations as opposed to actual biology) [see https://www.researchgate.net/publication/308756008_Clinically_significant_cardiopulmonary_events_and_the_effect_of_definition_standardization_on_apnea_of_prematurity_managementfor example]. My experience has been that the biggest issues are not, at their heart, technological but social and professional: We get parents who stare at the bedside monitor for weeks on end and are terrified to go home and we also get bedside nurses who either document every time the monitor alarms (often without enough context overnight for the team the next morning to figure out if the baby is actually any different) or nurses who document only the most severe episodes when a kid is getting ready to go home. One of my prior units started a program to standardize the approach of our nurses to these cases and, from a physician perspective, it Wass an unbelievably positive change

No, but we will give bolus surfactant (RDS dosing) after pulmonary hem. with hypoxia

Helsinki? Finland is the happiest country per the UN Happiness Report

2 weeks

Yes, we are in USA (3 different states I have practiced in)

We generally don't, for a combination of economic, physiologic and logistical reasons (in the USA). The reality is that our payers (private and even state insurance) will cover prolonged hospitalization for apnea so there is no financial pressure to discharge while apnea is a serious concern. Given this, we have a unit protocol that waits 5 days after any (unprovoked) clinically significant cardiopulmonary event (CSCPE) and 2 days after provoked events (usually feeding related). See https://www.ncbi.nlm.nih.gov/pubmed/27684421 for our standardized definition of CSCPE. There is weak evidence that there may be recurrent 'spells' even if a baby is spell free for 5 days (I can't find it at the moment, but there was a creative study from Virginia and Dartmouth a number of years ago that found recurrent spells unto 7-8 days after the previous event) but we've not seen this in practice. Finally, there are logistical barriers in our current environment: Our NICU clinic does not have staff/equipment/training to interrogate these devices. Our pulmonology colleagues do but they are very uncomfortable managing apnea of prematurity. The end result is that if we send babies on on such monitors and they go off the parents have no one to speak with who both understands the monitor and the underlying pathology and if they come to the ED no one will be able to interrogate the device in a timely manner. Furthermore, if the baby goes home on room air, there is no intervention the parents can offer if the monitor goes off except perhaps stimulation. Are they expected to stare at the monitor around the clock and swim the baby when it goes off? This way madness lies! When you combine these, I can recall sending ONE patient in 3 years home with such a device (not counting babies on home O2 who go home with a monitor for somewhat different reasons). It was at parents insistence and some deal brokered with the primary team that the covering weekend attending would discharge on a monitor. The baby was readmitted to our quaternary referral NICU for a blue spell at home within a week and it was a huge issue; I honestly cannot ever see myself sending a baby home on RA and with a monitor.

Yes; I'm familiar with its use in this context from a cardiac unit I used to work in and I know it has been used in PICU for refractory hypotension with at least case reports of success, but I have not seen any data for use in neonates. When I have proposed its use in extreme cases in my current NICU, everyone is concerned that the nitric oxide inhibition will precipitate pulmonary hypertensive crisis.

I suspect this is not a 'solved' problem in any of our units. I was recently on overnight with a similar baby and we were on Milrinone and Epi (maybe some dopa as well, can't remember details now); had a long conversation with our cardiac ICU about swapping out at least some of the Epi for Dobutamine one I had an ECHO with confirmed EF ~10-15% but this was very controversial (for reasons that were not very clear to me) and I was only on overnight, so I deferred to the primary team in the morning. Again, having just cared for such a case, when we have serial OB growth US and can see the weight trajectory prior to the fetus becoming hydropic, we estimate the non-edematous BW and make our initial dosing on that. Given that we subsequently follow urine output, weight and drug levels (where appropriate) I'm not sure that in practice we gain much from this exercise except that, perhaps, on the first day we are much tighter on fluids than we might otherwise have been.

This has been roughly my experience in3 different surgical NICUs in US