bimalc

The data is fairly clear that routine checking of gastric residuals is neither sensitive nor specific for serious pathology (aside from possibly enteric tube placement). The practice is associated prolonged time to full enteral feeds which itself is associated with a number of downstream consequences (increased central line days, extrauterine growth failure, LOS, etc.). While the Cochrane reviews indicate these secondary effects are uncertain, the preponderance of evidence favors either no difference or favors not checking.

Is there an error in the patient age or diagnosis? I can count on one hand the number of 3 year olds I have cared for in a NICU and collodion babies shed their initial dermatological findings in 1-3 weeks depending on etiology (at which time fluid management is much easier).

My current units do not admit babies who have been home for exactly the reason @Stefan Johansson said. However, I trained at two children's hospitals that did admit such babies. The mainstay of therapy is supportive care: positive pressure as needed, vigorous airway suction, recognition that apnea is common in RSV with neonates and that intubation can be more challenging than 'typical' neonatal intubation because these patients are often much larger than what we are used to (and thus good access and premedication for intubation under controlled conditions is VERY beneficial). Of the listed inhalation therapies hypertonic saline can perhaps shorten length of stay by <1 day. When the diagnosis is known (and assuming this is a previously healthy term baby) there is little indication for albuterol/atrovent (except maybe albuterol for bronchospasm after hypertonic saline). Sorry, not a lot of data, just anecdote.

No, but I feel the need to point out that (part of) the rationale for acetate in PN for premature infants is not for base infusion, per se, but rather to displace chloride and avoidance of iatrogenic hyperchloremic metabolic acidosis which is obviously a completely different problem than the bicarb infusions discussed in this thread. Contrary to the presented data that bicarb infusion is useless, there is a reasonable amount of data (though less for premature infants) that hyperchloremia is quite harmful. I'm not aware of any data arguing against acetate in parenteral nutrition for displacement of chloride. My experience is that it is almost never required and the handful of times I have done it I doubt that it is of any value. On the contrary, I have found that with appropriate fluid/volume management, aggressive use of acetate in parenteral nutrition to limit chloride infusion and good renal protection, metabolic acidosis is easily managed in all but the most extreme cases.

I cannot access the full text from home, but it strikes me that intermittent hypoxia is, at best, a surrogate for the clinical indication I and my colleagues have done trials of post-pyloric feeding in this patient population. As you say, practices vary, so perhaps I'm an outlier, but I use post-pyloric feeding for the very specific subpopulation of BPD patients for whom I am trying to modulate the mode of support (eg wean the baby who is 'stuck' on a low level of CPAP or a HFNC from positive pressure to a low flow canula that can be weaned on an outpatient basis). These trials of post-pyloric feeding typically run ~1 - 2 weeks and the outcomes we follow are (in order from least to most important): intermittent hypoxemia, baseline FiO2 changes, changes in level of support. I agree that those who seldom or never resort to transpyloric feedings need not change their practice based on this study, but I'm not sure this trial addresses the way transpyloric feeding is used in my part of the world.

Not routinely, but for high risk extubations we often coordinate with ENT and make plans for things like race epi at extubation to Heliox. I've also used it many times as rescue therapy when there is post-extubation stridor and I am trying to buy time for airway steroids to kick in.

There are several articles describing its use for this purpose and I would agree that it has very desirable properties. Sadly, not stocked by pharmacy at the institutions I have worked at recently.

I haven't used morphine for intubation in almost 10 years. The onset and duration of fentanyl are overall more desirable for purposes of intubation.

Because they relied on nurse charting of changes in vital signs, there was almost certainly non-differential misclassification leading to significant bias of effects towards the null. Nurse charting of events like desaturations is notoriously uneven relative to continuously measured data from monitors (this is one of the rationales for using SpO2 histograms to drive management instead of 'event counts'). A trial with continuous VS capture would best resolve the issue.

I would urge caution in assuming that tight glycemic control improves patient centered outcomes, though certainly, it would appear that if one were to test that hypothesis, it might be worthwhile to test it using such a closed loop system to give the intervention the best chance at success.

I've come late to the conversation after being on vacation and of course the dx of pneumatosis is not in question. I am, however, interested in the recommendation for surgical consultation: What is everyone's threshold for consulting surgery in NEC? Frankly, if I did not need to worry about my relationship with the surgeons more generally, I would only call them if I thought ex-lap or a drain made sense. This was the practice at the last in-born ICU I worked in whereas as the outborn unit I last worked in every child with NEC got a surgical consult. The difficulty with this was that the surgeons would then insist on driving the decisions on abx and NPO

I've used roughly the same thresholds as Hamed, fudging a little higher or lower based on symptoms. In addition to the collateral information Hamed recommended, the single biggest thing to figure out (in my experience) is whether this is iatrogenic or not. Often times, iatrogenic hypercalcemia even at high levels, can self-correct whereas if there is a real underlying cause, that too can suggest definitive therapy. Assuming it is not iatrogenic and the Family history is non-contributory, I would at least consider a diagnosis of William's Syndrome.

I practice in two very different ICU environments, one delivery and one which is more of a med-surg ICU closer to a PICU than a NICU in many ways. I think the data are clear and many of the previous respondents concur that NaHCO3 in the delivery setting is at best useless. For the ELBW with anticipated renal losses NaHCO3 should almost never be needed because these losses can be anticipated and should be incorporated into nutrition to avoid the biochemical inevitabilities noted in the articles Stefan cited. I suppose I might use bicarb in the preemie population if I had metabolic acidosis and evidence it was effecting cardiac output and even then I probably would not correct past 7.2. However, in the case of the older child or the med-surg patient where some specific pathologic perturbation has led to rapid collapse and I suspect part of that mechanism is bicarb deficit, I would have no hesitation to rapid correct the pH. I have several times done this and watched the EKG improve in real time.

When I was a fellow, I trained at a delivery hospital that used flow-inflating bags and it made this sort of failure very easy to recognize (if there was any defect in flow, the bag would not inflate). The downside to this is that without flow you can't give ANY respiratory support (after a critical incident of this kind where the flow inflating bag actually ripped in the middle of a resuscitation, we started stocking an emergency ambulance bag as back-up).

The UVC is clearly malpositioned. We could have an academic discussion of what vessel you've ended up in, but that thing is never going to get to the IVC/RA junction. It is also worth noting that the enteric tube appears coiled on itself also needs to be adjusted. Just curious, but was the indication for line placement?