bimalc

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.

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?