Therapeutic Hypothermia: not a panacea

Posted on 11 October 2013 by Keith Barrington

If hypothermia protects the brain, maybe we should use it for anyone who is at risk of brain injury during acute illness? Fortunately other potential uses of hypothermia are being investigated, such as this:  Mourvillier B, Tubach F, van de Beek D, et al.: Induced hypothermia in severe bacterial meningitis: A randomized clinical trial. JAMA 2013:-

100 comatose adults with meningitis were randomized to either cooling to 33.5 degrees or not. The study was stopped early as there seemed to be more deaths in the hypothermia patients. The early stopping could be criticized as the p-value was only 0.04 at that point, but it is always a difficult decision to stop early for a very serious potential complication, do you go on and confirm the complication but have more patients suffer, or continue and find that it was just a statistical fluke, or stop the study and risk being inconclusive, which means the included patients have not been able to contribute to the body of knowledge which was why they volunteered in the first place.

Anyway final analysis shows that the difference in death was non-significantly increased after correcting for other factors. The authors analyzed their data as best they could and concluded that there was very little likelihood that cooling was beneficial.

So it looks like we should avoid it in meningitis, and it is quite uncertain in brain trauma. Acute global hypoxia/ischemia in adults and term newborns is the only clinical situation where it is proven to improve outcomes. Before we start using it for necrotising enterocolitis, for example,  we need the kind of scrupulous study that the French multi-center group did for meningitis… and we need to figure out stopping rules first.

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Comment on my last post

Posted on 7 October 2013 by Keith Barrington

Please go see the comment from Alyssa Kent on my last post. Link is here. Alyssa is the mother of Virginia Kent, an extreme premie, and her insights are very provocative.

I like the term extreme premie, makes it sound like extreme sports, like jumping out of  a plane with a skateboard or something.

Also you can support the March of Dimes and Alyssa’s involvement with the Elm City Legends event.

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Variation in care for extremely preterm infants

Posted on 7 October 2013 by Keith Barrington

One of the things that is striking in neonatology are the variations in outcomes of the most immature babies. In some centers, and in some countries, when a mother presents with threatened delivery at what the doctors think is 23 or at 24 weeks gestation (which we don’t actually know very precisely) the babies are not offered active care. Other places discourage active intervention, while others are more open, or actively encourage institution of life support.

Not surprisingly if you don’t offer intensive care the babies die. Then you can honestly go to the parents and say ‘we don’t offer intensive care because all these babies die’. On the other hand if you are active at 24 weeks gestation, then overall survival can be over 2/3. Then you can go to the parents and say ‘we routinely start intensive care because the majority of the babies survive’. So the attitudes of the caregivers are the greatest single factor influencing survival rates.

As John Lantos has asked ‘why is this tolerated? If the same was true for breast cancer survival there would be a national/international outcry.’

Four recent publications all address this issue.

Mehrotra A, Lagatta J, Simpson P, Olivia Kim U, Nugent M, Basir MA: Variations among us hospitals in counseling practices regarding prematurely born infants. J Perinatol 2013, 33(7):509-513. In this questionnaire study the authors asked at numerous hospitals a series of questions about the antenatal counseling service. Who does it, when do they get asked to see the patient etc. They showed that antenatal counseling is universally available in tertiary hospitals for mothers who a threatening very preterm delivery. Apart from the lack of standard approaches and the rather surprising and worrying fact that obstetricians and Ob residents do a fair amount of the counseling sessions, their was a lot of variation in the earliest gestational age at which a consultation will be requested. More than half do not ask for a consult at 22 weeks.

This is of course related to the next study, Arzuaga BH, Meadow W: National variability in neonatal resuscitation practices at the limit of viability. American journal of perinatology 2013. Individual neonatologists were asked whether they would intervene in a number of different situations, at different gestational ages and birth weights and so on. There were substantial variations in practice that varied according to where in the USA they practiced. Practices were not much affected by religion, and there was quite a lot of variability.

Alleman BW, Bell EF, Li L, Dagle JM, Smith PB, Ambalavanan N, Laughon MM, Stoll BJ, Goldberg RN, Carlo WA et al: Individual and center-level factors affecting mortality among extremely low birth weight infants. Pediatrics 2013. I already discussed this paper in a previous post, but the point today is that there is a great deal of variation between centers, even those that you might expect to be a bit more homogeneous, US teaching hospitals in the NICHD neonatal network. Much of the variation in survival in infants less than 25 weeks gestation seemed to be associated with variations in the use of certain interventions, and the variations in survival were enormous, for all babies less than 25 weeks, survival ranged from 10% to 72%!

Serenius F, Sjörs G, Blennow M, Fellman V, Holmström G, Maršál K, Lindberg E, Olhager E, Stigson L, Westgren M et al: Express study shows significant regional differences in one-year outcome of extremely preterm infants in sweden. Acta Paediatrica 2013. And to show this is not just a US phenomenon, this regional study from Sweden showed variations in Obstetric interventions between regions of Sweden, and variation in neonatal interventions, and in infant survival. Most of the differences in survival were very early after birth, so they mostly probably were a result of decisions to intervene or not. So the proportion of babies at 22 to 24 weeks gestation who died before 12 hours varied from 11% to 46%.

I wonder what would happen if I went to a doctor with my skin cancer, and he told me, ‘on the other side of the river they treat this actively and you would have a 50% chance of survival, over here we don’t think that 50% is good enough, so we don’t offer treatment. But we can make your death painless, we have become really good at palliative care’. Not only would I be out of there like a shot (and I bet that doctors who discourage active care at 24 weeks would also be out of there fast) but I would make sure that there was some sort of investigation of why patients were being allowed to die just because of the doctors beliefs.

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The Microbiome and NecrotiSing Enterocolitis

Posted on 6 October 2013 by Keith Barrington

Fortunately Pubmed speaks both English and American, if you search on Pubmed for necrotizing enterocolitis it also gives you articles about correctly spelt gut diseases in preterm infants as well. As a North American transplant my spelling has become a bit haphazard, so sometimes its hemoglobin sometimes haem…

This fascinating new article has examined the development of the stool microbiome in preterm sets of multiples. I was delighted to read that the stool was ‘salvaged directly from the nappy’ from 12 sets of twins and 1 set of triplets from birth until discharge.  Stewart CJ, Marrs ECL, Nelson A, Lanyon C, Perry JD, Embleton ND, Cummings SP, Berrington JE: Development of the preterm gut microbiome in twins at risk of necrotising enterocolitis and sepsis. PLoS ONE 2013, 8(8):e73465 (free access). Basically the authors took the stool, (and also some breast milk) extracted DNA, amplified the 16S rRNA gene and then figured out what kind of bugs were present; on a subset of samples they did pyrosequencing to get more detail (if that sounds like I know what I am talking about, I do a bit. We are currently collaborating with Kelly Grzywacz, a fellow in peds GI, and doing some similar stuff in a lactoferrin trial, we do unfortunately have to use diapers, we couldn’t get any nappies. More on that study when we get to publishing our results).

Twins had intestinal colonization that was more like their co-twin than the unrelated babies. They were also more like their own mother’s breast milk microbiome than other breast milk. One of the babies developed NEC, and 5 days before that the microbial diversity became much less, and was then significantly less diverse than the co-twin. The co-twin also had an episode of getting antibiotics, which led to a smaller reduction in diversity which then recovered.

There have been other studies showing similar things in the past as noted in a review article last year, although not all the studies have shown the same thing. They consistently show changes in the microbiome prior to development of NEC.  Wang Y, et al. (16s rrna gene-based analysis of fecal microbiota from preterm infants with and without necrotizing enterocolitis. ISME J 2009, 3(8):944-954.) also showed a reduction in bacterial diversity. Whereas Josef Neu’s group showed a change in bacterial patterns and the appearance of a new potential pathogen, but no loss of diversity.

It seems from this new study that a baby’s gut colonization is strongly affected by the mother’s microbiome, particularly the microbiome of her milk, more than the environment of the NICU, but then we can really mess that up with antibiotics.

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Not just a diagnosis; a baby, with a family.

Posted on 4 October 2013 by Keith Barrington

A new publication in Acta Paediatrica is written by 3 mothers (Thiele P, Berg SF, Farlow B: More than a diagnosis. Acta Paediatrica 2013 seems to be open access). All 3 of them have previously written about their experiences with the medical system following a diagnosis of a serious chromosomal abnormality, and the lack of support and compassion that they confronted. But no, I am not complaining about duplicate publication! I think these 3 highly educated and articulate women have experienced attitudes that remain unfortunately widespread, and their stories deserve the widest distribution. These 3 women, 3  mothers, are from 3 different countries on 3 different continents. But they have all experienced the same lack of comprehension and lack of, sometimes refusal to, help. The common thread in their stories was that they valued the life of their child, even though they knew that life would have serious limitations and would probably be very short. They valued the life of their child even though they had a diagnosis that has been referred to in the past as ‘universally lethal’ and even though some physicians have decided that instituting active care is ‘clearly against the child’s best interests’ and that physicians who do so are ‘abdicating’ their ethical responsibilities.

The mothers point out that they want, and have a right to expect, an approach to the care of them and their children which goes beyond identifying the diagnosis and then deciding that all children with such diagnoses will not receive medical interventions. I have been privileged to learn from these women and others with similar stories; it seems to me that all they want is to be treated, and have their children treated, as individuals. To have their wishes, desires, hopes, and values listened to and considered, to have all reasonable options explained and then take a decision, open and transparently shared with their caregivers.

I mentioned in a previous blog that I think that attitudes are changing, one of the comments that was left was ‘not here they aren’t!’ But because attitudes may be changing, that certainly does not imply that they are anywhere near what they should be, or that all caregivers are going to become thoughtful, compassionate and supportive.

Often parents have been told that ‘there is nothing that we can do for your baby’. Annie Janvier and Andrew Watkins have written an article accompanying the mothers’ stories (which also seems to be free access) in one section of it they talk about that frequently heard statement:

There is always something we can do. For some extremely fragile children with several major malformation and /or low birth weight, [life sustaining interventions] can indeed be quantitatively futile, but we can always be there to support families in these tragic moments. We can guarantee that we will do everything in our power to treat any pain of discomfort their child may have. We can tell parents that the most important thing is that this child has parents who care and love him. That we also hope that they will meet their child and be a family for a while. While it is important to not give unrealistic hopes to parents, we can assure them that we will do everything for their child to have the best life possible.

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Informed consent in the NICU

Posted on 26 September 2013 by Keith Barrington

I have watched most of the presentations at the OHRP meeting, so you don’t have to. Many of the critics of SUPPORT make the same mistaken assumption, that usual care in the NICU is to individualize oxygen saturation targets, I don’t understand why these people (in addition to the people I have criticized before, there are 2 adult ICU docs, and the founder and president of something called the Alliance for Human Research Protection, Vera Sharav) couldn’t be bothered to actually ask someone who knows?

I wouldn’t go to a public meeting to criticize a research project in adult hematology and state with confidence that there was no usual care arm in the trial without talking to someone who knew what usual care was! One of the adult ICU docs gives the example of a baby on high oxygen that has a saturation of 92% and states that the usual response would be to reduce the oxygen saturation goals in order to reduce the oxygen exposure. I don’t know how he practices, but I certainly don’t do that. I also didn’t do that for the 15 years that I worked in the PICU either.

Lois Shepherd, another JD who is a bioethics specialist, in her presentation states something like ‘some defenders of the SUPPORT consent forms think that standard of care research means that the study is comparing 2 interventions that are commonly used and within the bounds of good medical practice’ she goes on to state ‘the SUPPORT trial would not fit within that definition either’. As is usual for such comments, she gives no reference or data, but just makes the assertion. She is, of course, wrong.

Some of the presentations, such as the one by Professor Annas, really suppose that the patient is an independent agent who seeks a medical opinion to determine which treatment to have. In such a circumstance they have the right to examine the options available with the various risks and benefits of each alternative. It is based I think on the model of the adult getting a consultation in a doctors office, the one-on-one decision making that is familiar to anyone who has watched doctor movies from the 50’s. The team I lead in my NICU consists of around 500 people (nurses, auxiliaries, RTs, clerks, cleaners, doctors at all levels of training, professionals in other fields as well) who are responsible simultaneously for around 65 babies. A good proportion of those babies would be dead if it were not for the NICU.

In that situation, the model of informed consent, which is so crystal clear to Pr Annas that he doesn’t really understand the controversy, starts to become really murky. Each day on rounds, for a particular patient I might make 10 different decisions, about the rate of feed increase, and when feeds should be enriched; about whether we will wean the rate of the ventilator or the pressures; about whether I will stop the antibiotics, continue for another 3 days, or do a CRP to help me make the decision; about whether I will ask for an echocardiogram, and if the PDA is indeed patent will I start treatment; and so on and so on. I try to make those decisions based on the best available evidence, and to weigh up the risks and benefits of each alternative. Many of the decisions are guided by protocol, because there is some evidence on which to base a protocol, or if not, the protocol is in place because we just want to make an arbitrary agreement. So our feeding guidelines are a protocol for the commencement and advancement of feeds in preterm babies. Most often the protocol works fine, and I do not adjust it, on some occasions I will decide to change the rate of increase of the feeds for certain clinical reasons.

Maybe Annas and Lois Shepherd will consider me negligent, but I do not discuss most of those options with the parents! Most of those day to day decisions if there is no unit protocol are made based on best guesses, minimization of harm, etc. Each of them might indeed carry risks and benefits that are different to the alternatives. When it is likely that a particular decision changes the risks of important outcomes, then I discuss with the parents. As I wrote several years ago, for example, before giving steroids to a child with severe bronchopulmonary dysplasia we should discuss with parents the possible long term consequences, as well as the short term benefits. As both are to some extent predictable based on published evidence (despite its limitations).

Our patients are often at nearly 100% risk of death if we do not intervene with intensive care, so, in our initial discussion with the parents we will often say that the patient may die despite our efforts. But death is rarely directly a risk of the treatment they are receiving, we dramatically reduce the chance of dying by instituting intensive care. So in the daily decisions about treatment options, if we do not know which of 2 options has the better chance of survival, then how am I supposed to inform the parents about the ‘material risk’ of death (which Dr Annas uses as an example of a risk that must always be disclosed)? For most of my decisions the risk of death is probably not particularly different between the alternatives but other important outcomes might be, and there will be some risk of death whatever I do.

If I were to design a trial to compare different feeding protocols, because I am truly uncertain whether one might be better than the other (and there are many, many different protocols out there), then I would do that because an evaluation of the evidence shows that use of either protocol would be an entirely reasonable clinical decision, even in the absence of the trial. Also, it must be crystal clear, if a baby is not tolerating their particular protocol, and I think they should deviate from it, then that is what happens. Research or no research.

Some of the presentations at OHRP such as George Annas and the entirely over the top Vera Sharav (who is tearfully outraged that we study fragile preterm babies) seem to think that we become unthinking, uncaring automatons, blindly imposing research protocols on our helpless patients the moment the misleading consent form is signed. Well, no. The parents assent to NICU care for their baby, and place a great deal of trust in me to make many hundreds of small and large decisions for their babies. Even some of the larger decisions, such as an intubation for surfactant, are not discussed with the parent beforehand to obtain their consent if it is clearly in the best interest of the baby. If a research protocol imposes a course of action that is not in line with those interests then we deviate from it. Without worrying about it. Every large study has some protocol violations, many of those are because someone in the team thinks the study directed approach is not consistent with the best interest of the patient. Even after informed consent for the trial.

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Prebiotics, to support growth of Probiotics, and how to kill them

Posted on 25 September 2013 by Keith Barrington

Ishizeki S, Sugita M, Takata M, Yaeshima T: Effect of administration of bifidobacteria on intestinal microbiota in low-birth-weight infants and transition of administered bifidobacteria: A comparison between one-species and three-species administration. Anaerobe 2013, 23(0):38-44. In this study the investigators report 3 sequential periods in their NICU, one without probiotics, one with one strain of bifidobacteria (breve) and one with 3 strains of bifidobacteria (breve, infantis and longum). They gave 5 x 108 bugs for each strain so the last group got 3 times as many. The babies were 1 to 2 kg and feeding by 7 days of age, and got the germs for 6 weeks. They looked at the microbiome with culture rather than molecular techniques and found there was better bowel colonization with bifidobacteria when the mixture was used than the single strain. Also there were fewer clostridia when either probiotic regime was used, and fewer enterobacteriaceae with the mixture.  It was a small study with about 14 babies per group, so no clinical differences would be expected.

Serce O, Benzer D, Gursoy T, Karatekin G, Ovali F: Efficacy of saccharomyces boulardii on necrotizing enterocolitis or sepsis in very low birth weight infants: A randomised controlled trial. Early Human Development 2013. This is the second published randomized study of saccharomyces, a probiotic yeast, in preterm infants, showing no benefit on NEC or sepsis. This could be a problem of power, as there were ‘only’ 208 babies in the trial and a lowish rate of NEC (7%) but it looks like we shouldn’t bother investigating single-strain probiotic administration with this yeast any further. I believe there is another trial that has been presented but not published as yet, also showing no benefit, but I don’t know any details.

Westerbeek EAM, Slump RA, Lafeber HN, Knol J, Georgi G, Fetter WPF, Elburg RM: The effect of enteral supplementation of specific neutral and acidic oligosaccharides on the faecal microbiota and intestinal microenvironment in preterm infants. Eur J Clin Microbiol Infect Dis 2013, 32(2):269-276. This was an RCT of prebiotic supplementation with the molecules noted in the title. They found that prebiotics in the milk did indeed increase intestinal colonization in 113 VLBW infants, compared to placebo. The biggest effect though was the use of broad spectrum antibiotics, which wreck all the bugs in the gut.

Gupta RW, Tran L, Norori J, Ferris MJ, Eren AM, Taylor CM, Dowd SE, Penn D: Histamine-2 receptor blockers alter the fecal microbiota in premature infants. Journal of Pediatric Gastroenterology & Nutrition 2013, 56(4):397-400. A case control study of infants from a prospective evaluation of normal microbiome development in the preterm. Of the 76 babies in the study there were 25 who had received H2 blockers for a mean of 19 days before the stool sample. None of them had recently received antibiotics. The babies that were on H2 blockers had less bacterial diversity, more Proteobacteria (some of which are bad)  and fewer Firmicutes (some of whom are good, including lactobacillae). The authors don’t talk about the Actinobacteria which includes Bifidobacteria.

As the authors state:

Many Proteobacteria, especially of the family Enterobacteriaceae, are known pathogens, such as Klebsiella, Shigella, Escherichia coli, Citrobacter … They are Gram-negative, facultative anaerobes, often motile, and capable of producing toxins, adhesins, and capsular antigens. They have the ability to undergo antigenic phase variation, type III secretion, and exchange antimicrobial resistance genes. Some have been associated with epidemics or anecdotal cases of NEC. An overabundance of such organisms in an immature GI tract is cause for concern.

I was happy to note tonight doing rounds, that, as usual, there isn’t a single preterm infant in the intensive care part of my unit who is receiving an H2blocker, or a PPI. Gastric acid is there for good reasons.

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Maybe CRPs are not CRaP? Not entirely convinced yet.

Posted on 25 September 2013 by Keith Barrington

This is  a nicely done study, with interesting data, but I am not sure I agree 100% with the conclusions.

Lots of newborn babies get antibiotics for suspected infection, they are usually stopped at 48 hours if the cultures are negative, which is much the most frequent outcome. New recommendations are to stop the antibiotics at 36 hours if the cultures are negative, and the baby is without signs of sepsis.

The authors of this study measured CRP with a bedside machine at 18 hours and then kept the results masked from the caregivers. The idea was to see if using a negative CRP was sufficiently predictive that antibiotics could be stopped earlier, after about 18 hours. There were preterm, late preterm and term babies in the study, 1202 of them. Which makes it quite big. There were 16 babies who actually had positive cultures. Which shows how many babies are unnecessarily exposed to antibiotics. In addition there were 107 babies who are called possible sepsis, as their mothers had received antibiotics and they were treated for more than 72hours. Most of the possible sepsis babies were probably not infected, but some may have been.

The CRP threshold that was used was 10 mg/L. Of the babies with an elevated CRP, only 14% had possible or proven sepsis, and under 3% had proven sepsis. Demonstrating once again the low specificity of CRP. There was only one infant with definite early onset sepsis who had a negative CRP, but another 43 who may have been infected, using their definition. Interestingly the negative CRP may be more useful for the late preterm and term baby, as all the babies more 34 weeks gestation who were asymptomatic at 18 hours of age and who had a CRP less than 10 were uninfected except one, whose mother had a positive blood culture.

The reason I say in the title of this post that I am not yet convinced is that it seems to me that there is a great risk that there will be unnecessary prolongation of antibiotic courses in uninfected infants if this becomes a routine. I am also not sure about the definition of possible sepsis, it is a real dilemma whether to start and or continue antibiotics in such infants. Many mothers are treated for fever, which becomes frequent the longer an  epidural is in place, many of the mothers don’t have a blood culture done, or other accurate investigations for serious infections.

Anyway overall this confirms what I thought about CRP, that they are very non-specific, but fairly sensitive. If you just focus on proven sepsis in infants who were 35 weeks or more, the sensitivity was 100%. I think it is likely that many of the ‘possible sepsis’ babies did not have sepsis, which is why there was little inflammation. They can be most helpful then in deciding to stop antibiotics (or sometimes making you feel more comfortable about a decision not to start them).

This study also makes me re-question the advice that I wrote about before from NICE, who suggest a CRP at baseline and then a repeat at 12 to 18 hours. I think this study suggests to me that the initial CRP would be a waste of time, if  you are going to do one, and you decide that a low CRP will change your management decision, then you should probably just do one, and do it at 18 hours after starting treatment.

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Fuzzy Images

Posted on 20 September 2013 by Keith Barrington

The title of this post I stole from the title of a newly published article (Mann PC, Woodrum DE, Wilfond BS: Fuzzy images: Ethical implications of using routine neuroimaging in premature neonates to predict neurologic outcomes. The Journal of pediatrics 2013, 163(2):587-592).

The commentary is a critique of the common practice of performing routine head ultrasounds in the first few days of life to predict long term outcomes in very preterm babies.

As I have noted here before, there is very little good data to support the practice. Head ultrasounds are poorly predictive of neurological or developmental problems, and are of no proven value for prediction of serious impairments.

In addition the large majority of studies that have compared head ultrasound results with outcomes have examined the children much too early to make good long term predictions, and (you might be able to guess what I am going to say next) a low 2 year score on the Bayley MDI scale is not an impairment! There is a recent meta-analysis of all the data that the authors could find comparing Bayley scores, mostly performed around 24 months, to later outcomes. They showed that the MDI correlated poorly with later testing, and that variation in MDI explained only 37% of the variation in IQ.

The commentary refers to one of the few follow-up studies of a largish cohort of very preterm babies who had intracerebral hemorrhages (referred to in the original article as periventricular hemorrhagic infarction, and in this commentary as grade 4 IVH) who examined the children at school age. That study from Roze and colleagues in Groningen in the Netherlands, including the extremely productive Arie Bos, showed that although many of the children had a diagnosis of cerebral palsy (16 of the 21 children) there were only 3 who had a GMFCS of 3 or worse. Meaning that the remainder were able to walk. Only 2 of the 21 had a cognitive outcome worse than 2SD below average. These 21 children were from an initial number of 38 infants who had periventricular hemorrhagic infarction, the remainder we are told ‘died in the neonatal period’. Now what that might well include are a number of infants who had withdrawal of life support because of the head ultrasound findings. It is possible that the infants with the worse appearance on head ultrasound were among that group, so we can’t in any of the studies really know what is the prognosis of all babies with this type of lesion, because there are some non-survivors in all of the studies, and it is rarely made clear if life support was withdrawn. In fact the group from Groningen have published a previous report which seems to include the infants in their newer paper, with a follow up to 24 months of age. In that paper they note that there were only 2 infants who died as a result of withdrawal of life support, so it is not such an issue for this cohort, but in some cohorts it could be much more important.

Despite that limitation there are now several studies that show very little effect of intracranial bleeds on outcomes of very preterm babies; including for example another paper by Roze and Bos, a study which followed 106 very preterm babies to school age, and showed ‘The children with cerebral lesions (grade III intraventricular haemorrhage and periventricular haemorrhagic infarction) had similar scores to those without cerebral lesions on total IQ and the Movement ABC’. Also interestingly ‘IQ scores did not correlate with gestational age’ the babies who were born at 24 and 25 weeks had scores not different to more mature babies.

To go back to the commentary by Mann, their introductory section ends with this sentence

We encourage neonatal practitioners to reconsider whether the perceived screening benefits are valid and the prediction of NDI definitive.

I think they present plenty of reasons to make that sentence much stronger: ‘screening head ultrasounds are of no proven value as predictors of important neurological or cognitive impairments, and it is therefore ethically questionable to use them for decisions regarding life sustaining interventions.  They should be performed only to screen for treatable lesions such as post-hemorrhagic ventricular dilatation.’

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Nous sommes à la télévision!

Posted on 20 September 2013 by Keith Barrington

Yesterday evening on “télé-québec” the first 22 minutes or so were about prematurity; it was all shot in our NICU, and features several members of the team here, nurses, a nurse practioner, neonatologists, RTs and parents. It think it turned out well.

If you want to watch the link is below, although you may well have to sit through an advert when it starts, it is also all in French.

Un reportage sur la prématurité, émis hier soir sur la chaîne ‘télé-québec’. Filmé dans notre unite à Sainte-Justine. Lien en bas, peut commencer avec une publicité.

http://zonevideo.telequebec.tv/media/6912/naitre-a-24-semaines/une-pilule-une-petite-granule

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