bimalc

I fear I may have exposed myself poorly. My concern is less with a ceiling (which implies that I am opposed to escalating levels of care) as opposed to walls or boundaries. By this I mean, my concern is that we sometimes offer families options which have no realistic hope of helping the family achieve their goals of care all because we do not wish to be paternalistic.

This is an important topic, but also one where national/cultural norms will have a large influence on practice. Coming from the United States, where a stated standard of shared decision making often is felt to devolve into 'the customer is always right', I have found that the single most important thing I can communicate with the team (either the ICU team I am leading, or the one I am consulted on as a member of my hospital ethics committee) is to remind everyone that not only do we have no ethical obligation to offer/perform non-helpful interventions, to do so is often unethical, especially when those interventions are invasive and/or traumatic. In the US, we often have the problem of feeling like we must ask the parents about every decision we make when, in reality, if there is no actual choice to be made we ought not to offer a false choice (and then get mad at the family for choosing incorrectly).

Given that ELBWs get comprehensive follow-up (at least in most settings I know where you could even contemplate routine MRI at discharge), what possible value could MRI provide which would change care or outcomes? Would you stop following up ELBWs who you 'knew' by imagining criteria were not going to have CP? I doubt it, because you'd want to see them anyway for other developmental reasons. Do you have an intervention which can prevent CP after NICU discharge? I don't. The best you can say about a routine MRI protocol is that you could tell the parents on graduation the probability of their child developing CP. That prediction is only reasonably reliable for a 'normal' study and in either case isn't really much better with MRI than with US. Maybe this will change with research, but I'm pessimistic. Research will probably make imaging a better research tool and inform our understanding of brain development and injury, but the clinical utility of making predictions at NICU graduation, in the absence of some sort of specific post-discharge intervention, seems dubious at best.

I was unaware anyone was arguing that 0.5mcg/kg/dose reliably provided any clinically meaningful effect in the context of direct laryngoscopy. There are, however, doses of fentanyl between 0.5mcg/kg and 5mcg/kg which almost certainly offer some analgesic relief and (at least as importantly) provide a side effect of sedation which improve intubating conditions while not so suppressing respiratory drive that extubation becomes impossible.

The practical problem with this claim (which I think we all believe in in principle) is that, at the time the initial plan for the day is made, TPN must be ordered and a fluid goal set. In the setting of MEF, you have no sense of how much will be tolerated and absorbed, whose belly will blow up, etc. As a practical matter, one has to simply assume that volume does or does not 'count' and accept that you will be 'off' in one direction or another. It actually does not matter, as long as one is consistent within the unit and if there is ambiguity when sharing with other units, that you are clear on what your practice is. As long as all sides of a discussion understand the chosen convention, you can have an informed discussion about the specific needs of the patient and any needed changes in the plan over time. My experience in 5 NICUs over the years is that none has counted MEF towards calories or volume and instead relied upon TPN to meet all nutritional needs during this period. Again, for ease of computation (and thus safety) the practice in ICUs I've worked in (and a practice I subscribe to) is that once you are past MEF you are implying a belief in physiologic tolerance of the feeding volume (otherwise you would not be ordering feeds) and so you should count all the volume/calories.

I have no idea what the cost is, but intranasal fentanyl could be an option. I've only ever used it in a palliative setting, but all out babies who would be insure candidates are getting IV placed for fluids. Even with aggressive enteral nutrition we used a few days of fluid.

I have never practiced with a group that did INSURE, but I've often wondered about premedication, especially after the study from Albany with an astonishingly high failure rate when using morphine as the premedication. Helpfully, that same group now provides data on use of remifentanyl instead: https://www.ncbi.nlm.nih.gov/m/pubmed/29789465/ Personally, the biggest change for me once we go to INSURE (assuming we don't just skip to MIST/LISA) is that I've routinely muscle relaxed for intubation for a number of years.

I also have an exceedingly low success rate in SUA cases (I am credentialing at a new facility and reviewed 3 years of my umbilical lines and I had only one successful UAC in SUA listed over a 3 year period)

The approach these authors suggest is really only implementable for moderate to late preterm infants. The overall approach is tempting to extend to more extreme premature infants, but I'm not aware of anyone pulling together the data to do this (Presumably the NRN in the US has the underlying data and VON may as well, though both are limited datasets in terms of post-discharge data. CHNC has a much higher risk and outworn population but does have a validated PHIS linkage as well as (theoretically) neonatal follow-up data). Stefan - when you say individual fortification, are you looking solely at patient characteristics or are you assessing (for milk fed babies) the caloric density and relative macronutrient composition of the milk (mother's own or donor) in order to guide degree of fortification? At the Pediatric Academic Society Meeting in the US this year there was a Swedish vendor (https://www.mirissolutions.com) selling an FDA-approved solution for human milk analysis: Do you have experience with this device?

I've never seen this, but my first instinct would be to work the child up for diabetes (assuming this isn't sepsis or iatrogenic). If a biochemical diagnosis was not immediately obvious and you are in the UK, I would see if the genomic medicine service in Cambridge would accept your patient for neonatal whole genome sequencing. In terms of actually lowering the blood glucose, you could try increasing protein intake (if calories are adequate already, you could even reduce carbohydrate calories). Branched chain AAs are a key signal for energy balance and can stimulate a more robust insulin.

I have never found the need to use the quantitative ratio of insulin and glucose concentrations (and I assure you, your lab is measuring an insulin concentration in the samples you provide. If you are getting reports of insulin levels that are not concentrations you need to call your lab director). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141553/ is a review that discusses one demonstration of a modified ratio as well as its limitations, though not in neonatal data.

What do you mean by 'early intervention'?

The use of a ratio without units implies that both quantities should be in the same units before taking their ratio. which units you choose to use is irrelevant. The purpose of the ratio is to detect inappropriately high insulin levels during hypoglycemia.

This is perhaps not the answer she was hoping for, but in her own multi center cohort study on bleeding risk and transfusion from 2017 there was at least one center that administered concentrated platelets ...

Thank you, Stefan, for reminding me of my one major criticism of the PINT trial: They did not include NEC (or at least surgical NEC) in their composite outcome. As for why we, as a profession, continue to worry about TANEC, it is mostly recall bias (we all remember the case of NEC shortly after transfusion but we never stop to think of all the transfusions we have given without NEC appearing) I've often wondered if there isn't already enough data out there to answer these questions (or at least get a start). Supervised learning techniques have advanced sufficient that if you were willing to invest in combining and curating multiple datasets of ELBWs you could probably train a binary classifier to predict risk of NEC with or without transfusion.

I would recommend reaching out to Susan.Slattery@northwestern.edu who helped develop weight-based standardized feeding pathways with me when I was in Chicago. The broad outlines of our approach were weight-based stratification, q12h advancement of volumes by nurses without waiting for the rounding team to arrive (in babies with expected course). When I left that unit, I think we were advancing ELBWs ~24mL/kg/d after a few days of trophic feeds, but I heard through the grape vine that they either slowed that down for all ELBWs or subdivided the ELBWs around 600-700g and slowed down just the absolute smallest babies, but either way, she would have the most recent information. Outcomes showing improvements in enteral nutrition without increased NEC were presented at PAS last year.

My differential in cases like this includes meconium peritonitis (obviously not what your baby has), infection/TORCH, chromosomal (quite common once you've excluded the previous two), Metabolic (Lysosomal storage disorders and peroxisomal biogenesis disorders most notably), endocrinopathy (primary or paraneoplastic) with ectopic calcification, vascular calcification (of which some may be due to mendelian disorders). Additional history I would request would be pregnancy exposures/infections and family history including potential consanguinity. In terms of ICU management, in resource limited settings, almost none of these evaluations need to be done in the ICU. Assuming the child was near intact and well appearing, feeding and otherwise ready to discharge soon, I would check an ECHO (if available) for structure, function and effusion and review X-rays for evidence of metabolic disease. The app face2gene has a function where you can upload X-ray images if you do not have local expertise in reviewing x-rays for these signs. You said 'labs WNR' but I would double check that the Ca and P were not borderline and in need of repeat before discharge, and that transaminases and the total and direct bill are reassuring. I would collect the relevant infectious studies during the index hospitalization, especially CMV, in order to better interpret congenital vs acquired exposures. Things you could defer to outpatient (many of which I would do in the US during the index hospitalization) would be karyotype or (preferably) microarray with SNP probes for potential regions of homozygosity, metabolic studies for lysosomal storage disease and peroxisomal defects, Endocrine evaluation of PTH axis, vascular imaging and consideration of related single gene disorders (most notably GACI, generalized arterial calcification of infancy).

I know this is not what you mean, but the single most common cause of this phenomenon in my experience is actually reversal of the probes (ie the pre- and post- are mislabeled/swapped). But, yes, I have seen several cases of the actual physical phenomenon you describe, often self resolved in a short period of time and sometimes causing an annoyed call from a cardiologist asking why I got an ECHO

The important thing is WHY you think these things are happening. If the patient is over breathing (and they presumably are at a RR 20) and they are generating some reasonable tidal volume natively, changing the rate is unlikely to help CO2 retention (though it might help work of breathing/retractions), similarly if you think the patient cannot natively generate sufficient tidal volume then increasing delta P and/or RR may be reasonable. Finally, recall that the single most important goal of respiratory support, especially early in life, is maintenance of functional residual capacity. If you think you are in respiratory failure because you are losing FRC, you need to re-recruit and increase PEEP (and possibly MAP more generally) to try and maintain FRC.

I am biased as I was a fellow in the NICU where these were tested/developed. In the short term, I think the biggest promise is in relatively stable/healthy babies where the wires freak out parents and discourage bonding. Probably need more work before they can be used in the micropreemies.

https://lifeinthefastlane.com/ccc/cvp-measurement/ I have mixed feelings in LITFL as they often just make a series of statements and then list some references at the end (as opposed to indicating in the text what evidence there is for each claim) but for this particular discussion, it seems like a reasonable starting point. I could caution that, as we always are, we remain skeptical about the extrapolation of this data to neonates (on the other hand, for many of these issues there is no neonatal data so one must start someplace).

It may or may not be applicable, but if you're setting out to use CVP monitoring in sick neonates, it might also be helpful to think about what things might change the CVP (other than what you're trying to measure). There is a robust literature in adults (and older children) looking at the effects of high PEEP etc. on CVP readings. I haven't looked at it in a number of years, but if I was going to start transducing CVPs regularly and getting calls from nurses or house staff about shifts, I'd probably want to have a mental list of all the iatrogenic things that can and cannot change the value of a CVP reading.

In my experience CVP is much more helpful as a trend - if I plug in the transducer and it says 8 vs 6, I'm not sure I know what that means. But if it was 8 all day and now it is 6 or 4, I can go looking for a reason for the change or a consequence of that change. If I'm looking for numbers to target early in the course and I'm worried about preload status, I'd much rather know targeted echo (if available at your facility) and/or pH and lactates.

Certainly I agree with @Stefan Johansson on the exception to the rule stated by @rehman_naveed. I have never done it, but I've at times wondered if I wouldn't give glucose gel a try in a situation where there was some difficulty obtaining access, just to get the sugar up a bit while I put in an umbilical line.

hi stefan, 1-2mcg/kg/dose given over 1-2 minutes (higher starting dose in non-opiate naive pt) repeat if needed + 0.1mg/kd midazolam (not used in preemies) + 1-1.2mg/kg Rocuronium (or Vec depending on what is in stock) [neuromuscular block being optional and requiring a fellow or attending at bedside to give]. I can recall only one incidence of chest wall rigidity having use this combination over a hundred times (with the caveat that over time I have come to almost universally give Roc/Vec). Regarding Ketamine, I have never intubated with it, but have certainly used it for conscious sedation. My concern would be what neurodevelopment effects Ketamine has on a preemie.