More thoughts about what to de-adopt

My post about de-adopting certain investigations or procedures in the NICU got a lot of suggestions and responses. Here are a few, either from the comments section or from Twitter. We should de-adopt the following:

  1. Dopamine. This is a suggestion that I have a lot of sympathy with, the 2 major actions of dopamine in the newborn are to cause vasoconstriction and to suppress the pituitary. I don’t think that vasoconstriction is often what we want when we initiate cardiovascular support. All the studies of dopamine with analysis of haemodynamics have shown that if you give enough dopamine to increase blood pressure then you decrease cardiac output. In the occasional baby with vasodilated shock, a vasoconstrictor might be useful, but other agents may be more effective. Dopamine suppresses release of TSH and thus thyroxine, also suppresses prolactin and growth hormone, these actions are probably not beneficial and are not shared by other catecholamines. (Dopamine also suppresses respiratory drive and is associated with an increase in nosocomial sepsis.)
  2. Supra-systemic hypertension to reverse the shunt in PPHN. This is related to the first issue, an older idea about how to improve oxygenation in PPHN was to push the systemic pressures higher than the pulmonary artery pressures. Dopamine, which was for a while almost the only vasopressor that neonatologists used, was shown to cause vasoconstriction in the systemic and pulmonary circulations. A study by Willa Drummond in lambs noted that when extremely high doses of dopamine were given, systemic vasoconstriction exceeded pulmonary (at 270 microg/kg/min), she reported using dopamine in human newborns at 20 to 125 microg/kg/min. The extreme vasoconstriction with such doses impairs myocardial function. A balanced approach, supporting the systemic circulation where necessary without excessive vasoconstriction, and dilating the pulmonary arteriolar bed if needed, makes much more sense.
  3. Hi-FLo. I think that High Flow Nasal Cannulae are overused, and there are some suggestions that centres that have adopted widespread use of Hi-flo have more BPD. Because they are comfortable and well-tolerated by babies and parents I think they tend to get weaned less aggressively, which might lead to more BPD diagnoses. However, I do think that nasal injury is important, and patient comfort and parental wishes are important, so I would say a partial de-adoption, rather than complete, is more reasonable, and don’t forget to wean them whenever you can.
  4. Gentamicin levels after the 2nd or 3rd dose. We have already done this, gentamicin levels in our NICU are only ordered if the gentamicin is continued after 36 or 48 hours, so usually only when the cultures are positive. Which doesn’t happen very often. I also agree that trough concentrations are not very predictive of anything. Vancomycin levels are a similar issue, poorly predictive of either efficacy or toxicity. I think we do many of these levels for medico-legal concerns rather than to help our babies.
  5. Sodium Bicarbonate. I absolutely agree, I have prescribed Bicarbonate once in the last 25 years, when I was being pushed to do so by a cardiologist, I re-reviewed all the data I could find after that, and I won’t be doing it again.
  6. Treating all PDA, or even doing the echo to diagnose them. The example in the tweet regarding echos was an infant on 21%, tolerating feeds and urinating well. This is such a complex issue that I will post something about it soon, in particular in response to a new publication from Montreal. But I certainly agree that many PDAs don’t need to be treated, the question is: which ones?
  7. Checking residuals and stool guiac. Checking residuals can be done away with without any adverse consequences. Routine stool blood testing should also be thrown out, occasionally if you are not sure that there is blood present or not, then maybe confirmation with an occult blood test might be helpful, but if you need the test there can’t be much blood there!
  8. Spironolactone (my own addition). I don’t think there is any indication for the use of this drug in the neonatal period. See my recent post on medication use in BPD.
  9. Long term diuretics to prevent or treat BPD (also my addition). No evidence of benefit, substantial evidence of harm.

And one suggestion from Gil Wernovsky on LinkedIn

Using the term “Pulmonary Hypertension” in isolation. Should always be qualified with 1. Elevated PVR 2. Low PVR with elevated PA pressure due to intrasvascular communcation. As Gil notes, sometimes we end up treating babies with high flow/low PVR pulmonary hypertension with pulmonary vasodilators, which is usually a big mistake! I agree with this: treatment of pulmonary hypertension should always take into account the pathogenesis and the haemodynamics. Discuss it with the cardiologist (just don’t give them bicarbonate; at least not the baby, a bit of oral bicarbonate for the cardiologist might help his dyspepsia).

Also this was a question rather than a suggested addition

Milk thickeners for reflux. There is very little good neonatal data about this, we know that some thickeners (or perhaps just one) have been associated with NEC, specifically Xantham Gum. So avoid that completely. Other thickeners may be safe, that is not clear, but they probably do have some effect in reducing the number of regurgitation episodes, and perhaps the overall duration of acid reflux on pH study. I would say milk thickeners in any baby at risk of NEC should be de-adopted. For infants past term who have major regurgitation and no other risk factor for NEC (not a gastroschisis or congenital heart disease baby) they might be safe and reduce the number of regurgitations. (see Cochrane review)

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. Bookmark the permalink.

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