bimalc

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.

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.

One thing to consider about this study (and the other published comparisons between NCH in the USA and UUCH in SWE) is that there are essentially no deliveries at NCH. These babies are born in the community (generally at hospitals with level 3 NICUs) and transported to NCH [I am unsure if the UUCH births were in-born or outborn]. I think the earlier study from Iowa in NEJM already demonstrated fairly convincingly that if you try you get better outcomes than if you don't, and there is a long standing literature on the differential outcomes of inborn vs outborn VLBWs but what remains unclear to me is what the magnitude of this effect is in 22-23 week infants and whether these differences are large enough to effect counseling in systems like the NCH one where active resuscitation also entails transport.

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.