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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 really liked this blog post! I guess many of us have seen devastating cases of post-transfusion NEC that stay with us  and  therefore add "bias" to our judgements on this topic. There are still questions though right? Like the severity of the anaemia (how low do we leave the Hb and is that threshold different for certain babies?), the duration of anaemia (how long do we leave it before we transfuse?) and then,  if the mechanism is a re-perfusion injury post-transfusion, how do we prevent it?!

Check out this blog post by Keith Barrington whether transfusions trigger NEC. Or does anemia. https://neonatalresearch.org/2019/04/16/do-transfusions-trigger-nec-or-does-anemia/  I would say that there are enough clinical research data out there to say that there seems to be NO association. Just check out the PINT trial, the RCT comparing a liberal vs a restrictive Hb level for transfusion in preterm infants. If anything, the more liberally transfused group of infant had less NEC. And read this paper by Patel et al that nicely demonstrates that there seems to be confounding of indication coming into play, i.e. it is not the transfusion but the underlying anemia is the problem. Despite research findings, this question (whether transfusions "lead to" NEC) is still troubling us. Why so?

Hi . the patient is already better. the problem was that it should lower the frequency to the maximum and return to high values of delta p. I think the problem is the draguer vn500 that is not powerful enough to ventilate a patient of 4500 gs by passing it to the sle500 put down the pco2

@juan carlos vidal sorry that I did not see that you posted this question in this thread - but have shared over our social channels now. Anyway, it seems that you have adjusted the HFV as possible, with reduced freq and a higher d-P. Does your ventilator give tidal volumes? What approx levels of PCO2 (kPa) do you have? Have you tested regular tidal support, like SIPPV?