PAS 2018: the wrap-up.

A general comment about these PAS 2018 blog posts. I think we should be very careful about changing practice based on an abstract. We should respect peer review, with all its limitations, and we should always consider new research in terms of the quality of the trial, and how it fits in to the overall evidence base that already exists.

Sometimes there is little that already exists, and you could say, for example with the SAIL trial, that if you have already started using sustained inflations in the resuscitation of very preterm babies then you should reconsider your approach and probably stop doing it, at least as a routine. This was a high-quality trial with no real previous data on the overall clinical outcomes with sustained inflations in this population.

In contrast  for propranolol use in early retinopathy, there are previous data, but they are limited and of variably poor quality, and the quality of this new small trial is difficult to determine from the abstract. I think it would be a serious error to start routinely using propranolol in this population, there are a large number of unanswered questions, and potential risks. It is a trial that should be used to give support to a large multicenter RCT.

STOP-BPD is somewhere in the middle. A high quality trial with important clinical outcomes, and nothing quite similar in the literature, but there are many other trials of post-natal steroids and some other relatively similar trials going on right now. My response will be to wait and see, and try and analyse how this trial fits into the totality of the literature.

There were many other presentations that I found interesting at PAS. A study from Alabama with Colm Travers as the first author (1413.115) showed that it is possible to predict bradycardic episodes in preterm babies with apnea by training a neural network on previous heart rate patterns that preceded bradycardic episodes. Once trained the network could predict when the next brady was happening. I wonder how this would work if you looked at respiratory patterns, I remember some articles from the 1980’s (Waggener et al for each of them I think) where passing respiratory signals through a comb signal demonstrated multiple, otherwise difficult to see, respiratory pattern oscillations. When all the different oscillatory frequencies were at their lowest at the same time the babies had apneas. There may be some relationship between these 2 findings.

Peter Dargaville from Hobart, Tasmania, had several posters/presentations about automated oxygen control. One of them in particular (1413.112, first author Andrew Marshall) relates a little to my previous comment, they added a trick to their oxygen controller that immediately starts to increase the FiO2 at the onset of an apnea (or about 5 seconds later), rather than waiting for the infant to desaturate. Using this trick the periods of time when the infants were hypoxic was shorter. In manual FiO2 control the hypoxia lasted 30 seconds, with standard automated control it was 20 seconds, and with the added apnea-response element it was 12 seconds.This is a great trick, but I am not sure its the right thing to do. Obviously if you are not breathing, increasing the FiO2 isn’t going to do anything, so they are doing this to get the babies to re-saturate faster when they start breathing again. Is that what we really want? Release of oxygen free radicals during re-oxygenation might be worse if you reoxygenate faster, and increasing the FiO2 during apnea often leads to post-apneic hyperoxia, (I published an abstract about that several years ago, and there has since been a full publication from another group). In this study they calculated the number of seconds multiplied by the saturation percentage above target range, and there was more hyperoxia in the 60 seconds after the apnea when the new apnea-response element was switched on. I have thought about this a lot in the past, I think we should have studies looking at the best way to intervene for apneas, maybe the best way to intervene would be to immediately start assisted ventilation with the same FiO2 that the baby normal receives, but after how long? Does stimulation work (I think it probably does) and should we give a transient increase in FiO2 during recovery, or not? How can we reduce post-apneic hyperoxia? Anyway, this is a really interesting study showing you can integrate signals of respiratory activity into the FiO2 controller.

The lucinactant study group is pursuing its studies of aerosolized surfactant. Neil Finer and colleagues (abstract 2899.821) performed this blinded study looking at 2 different doses of lucinactant (40 or 80 mg/kg) in babies 28 to 32 weeks who were on CPAP for HMD. 44% of controls failed CPAP and 32% of those who received 80 mg/kg of phospholipids by aerosolization. More work to be done yet, but this is looking interesting.

There was a good observational study on premedication for intubation from the NEAR4Neos database (abstract 1414.123, first author Yuri Ozawa). It confirms what some of us have been saying for years. Not only is pain relief the humane thing to do for intubation, adequate therapy, that is “sedation” plus paralysis, makes the procedure more likely to be succesful on the first attempt and associated with fewer adverse physiologic changes. In this abstract “sedation” meant a sedative or a narcotic, which I think is a mistake. Non-analgesic sedatives should not be used for this procedure, and the authors should divide the data into analgesic or anesthetic regimes on the one hand, and sedatives (such as midazolam) on the other. In this study babies who received only “sedatives” were worse off, with fewer 1st time successes and more desaturation. An observational study to be sure, so interpret with care.

I guess I could continue for a while, there was a lot of resuscitation research, for example, including several projects presented from Edmonton, in simulation, in animal models and in babies. If you go to the website and search for Georg Schmolzer under presenters you can find those. There were many interesting things about the microbiome in preterm babies also, under the “program” heading you can filter for microbiome, you will get 67 hits, but then finding the preterm stuff isn’t difficult.

I can’t see how to place a link directly to any of the abstracts, is the best I can do; this URL will take you to the welcome page, and you can then find the abstracts if you know the presentation number by clicking on program, then “filter” then typing or pasting the presentation number if you know it.



About Keith Barrington

I am a neonatologist and clinical researcher at Sainte Justine University Health Center in Montréal
This entry was posted in Neonatal Research and tagged , , , , . Bookmark the permalink.

2 Responses to PAS 2018: the wrap-up.

  1. Namasivayam Ambalavanan says:

    Hi Keith,
    As the senior author of Colm Travers’ abstract, I can add that we did look at respiratory rate and pulse ox tracings in addition to heart rate for the prediction of bradycardia (using the nonlinear autoregression neural network), and we did not see any improvement in predictive ability (probably because the predictive ability is already very high). We could predict apnea (not just bradys) but the identification of apnea on an electrical impedance signal is not very accurate. We are doing more in-depth work as part of the NHLBI U01 PreVENT consortium.

  2. Pingback: Surfactant by nebulisation | Neonatal Research

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