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Showing content with the highest reputation since 08/06/2020 in all areas

  1. 4 points
    https://onlinelibrary.wiley.com/doi/epdf/10.1111/apa.15495 With kind permission from Luigi Gagliardi. And as mentioned: the "official" accepted Ms. It is marked as "free download", so it is perfectly legal. (As soon as the final version is available, I will post the link )
  2. 3 points
    Friends, I am glad to share that an article of mine about racial disparities, titled 'I Can't Breathe' was just published. Here is the link to the full text of the article (the full text is not available if you go through the journal website). Please share widely - I hope it stimulates action by readers to reduce racial disparities in care and outcomes in the field of perinatal and neonatal care. https://rdcu.be/b6cgM
  3. 2 points
    We sometimes culture infants for herpes simplex born through a normal vaginal delivery and maternal herpes simplex is discovered late during or after delivery (typically recurring herpes). In case of a positive herpes PCR, for example in the upper airway, but negative PCR in blood and cerebrospinal fluid - how would you outline management How do you reason around "colonization" vs "infection" with herpes simplex? My experience over the years, is that a more active management are now adviced from our virology consultants, i.e. iv acyklovir for a relatively long time period.
  4. 2 points
    Considering hygiene you should not do it, but I do it 1. if I need a blood culture and the line may be responsible for the infection, 2. if I need blood and the PICC line is about to be withdrawn, 3. in emergencies. The technique is to withdraw with a 1 ml syringe using a constantly changing negative pressure of 0,5 ml maximum. Stop if the blood column does not move constantly (and slowly) and immediately flush with a prepared saline syringe. It works 90% of the time. Erythrocytes are a lot smaller (7,5µm) than the inner diameter of a PICC line (28G = 1Fr has 0,17mm = 170µm). A study has shown that you can give blood via a PICC line without hemloysis (Pediatr Crit Care Med. 2004 Jan;5(1):69-74. PMID: 14697112). See also nice experiments in https://chartermedical.com/wp-content/uploads/2015/09/TexasChildrensPDF.pdf. There it is stated that you should not do it with platelets because of clotting. In an emergency we gave 80 ml FFP via 28G PICC line with no problems. It needs a pump with pressure cut of set to max - you can not do it by hand.
  5. 2 points
    Intubate-Surfactant- Extubate or INSURE has been around for awhile. The concept is to place an ETT while an infant is first on CPAP and then after pushing surfactant in quickly remove the ETT and put back on CPAP. This does not always go as planned though. If after surfactant the FiO2 remains above 30% many people would keep the ETT in place as they would surmise that the infant would fail if the tube was removed. They would probably be right. Sustained inflations have fallen out of favour ever since the SAIL trial results were published and written about here . Having said that, the concept of using sustained inflation is to open the lung and expand closed alveoli to improve both oxygenation and gas exchange. Much like giving inhale nitric oxide to a collapsed lung is unlikely to make much difference, the question could be asked whether giving surfactant to a lung that is most collapsed will fail to deliver this compliance improving medication to the areas of the lung that most sorely need it. Our Italian colleagues therefore decided to undertake a study to look at providing surfactant to lungs after a recruitment manouver and see if this made a difference to the meaningful outcome of extubation failure after surfactant provision. The results are intriguing and as such here we go in looking at the study. Optimizing Lung Expansion The trial is the Lung recruitment before surfactant administration in extremely preterm neonates with respiratory distress syndrome (IN-REC-SUR-E): a randomised, unblinded, controlled trial and involved 35 NICUs in Italy. All infants enrolled were born from 24 + 0 weeks to 27 6/7 weeks gestational age at birth and all < 24 hours of age at enrollment. Each baby had to be on CPAP at the time of randomization and meet prespecified failure criteria of FiO2 of 0·30 or greater for target SpO2 of 87% to 94% for at least 30 min or in 10 Infants for rapid deterioration of clinical status or if pCO2 was > 65 mm Hg with a pH less than 7·20. Regardless of which arm they were randomized to all infants received 1-2 sustained inflation breaths using 25 cm H2O for 10-15 secs using a t-piece resuscitator after being started on CPAP as was the practice at the time. After randomization which could not be blinded, patients were then either given surfactant via INSURE without any further strategy for opening the lung or received the IN-REC-SUR-E approach. The latter involved putting the infant on high frequency oscillation starting with settings of mean airway pressure 8 cm H2O; frequency 15 Hz; ΔP15 cm H2O; and inspiration to expiration ratio of 1:2. Using this modality infants underwent stepwise recruitment methods prior to administering surfactant (poractant). The primary outome was the need for mechanical ventilation within the first 72 h of life. Infants met the primary outcome if they were not extubated within 30 min after surfactant administration or required reintubation before 72 h of life. The Results Based on a power calculation the authors needed 103 infants in each arm and they recruited 107 in the treatment and 111 in the control arm. In the per-protcol allocation 101 received the treatment and 111 the contol. While the strategies for extubation were not set out to be equal (units were allowed to extubate to anywhere from +6 to +8 for pressure levels), the groups were not different 7·0 cm H2O, SD 0·4 for the experimental group and control arms. Given the steps taken to open the lung in the lung recruitment arm, the FiO2 was lower at 28% prior to surfactant provision in the treatment group than in the usual INSURE approach at 42% prior to surfactant provision. All infants were extubated within 30 minutes of receiving surfactant. As the results demonstrate, whether there was an intention to treat analysis or per-protocol analysis the babies who received the intervention were more likely to remain extubated. The number needed to treat was 7 which is a pretty powerful measure. Interestingly, looking at secondary outcomes there are some interesting trends as well including less mortality which on a per-protocol analysis was significant but also a trend towards more PVL at 9% in the treatment arm and 4% in the control. The mean times to surfactant administration were 4 hours in the treatment group and 3 hours in the control but the high frequency manoeuvre had a mean duration of only 30 minutes. It is possible that the use of high frequency could have blown off CO2 to very low levels but I am uncertain if the short reduction in pCO2 could have contributed significantly to reduced cerebral perfusion if that trend is representative of something. Interestingly, pneumothroaces were not different between groups as no doubt as a reader you might wonder if use of high pressures to recruit the lungs when they are non compliant might have led to air leaks. So it worked, now what? First of all, the results to me make a lot of sense. Opening the lung before delivering surfactant and then seeing better chances of staying extubated doesn’t really surprise me. Some questions that come up now for me would be how this strategy would fare in those who are older at birth. I suspect given the greater chest wall support and lower likelihood of severe RDS this strategy might be even more effective at reducing FiO2 or perhaps CPAP need in terms of duration after extubation. I would think it unlikely to make a difference in reintubation though as most would remain extubated regardless. That is for another study though with a different outcome. There will be centres that don’t like the use of HFOV for recruitment so what other strategies could be used in lieu of this? I hate to say it but there will also be calls to have a much larger study specifically designed to look at the secondary outcomes. Would a larger study find a significant increase in PVL or demonstrate that it was just a random finding? Might mortality be proven to be lower and even more so? Regardless of the above what I think this paper does is give us reason to pause before giving INSURE and ask ourselves if we have done what we can to open the lung after intubating before rushing to squirt the surfactant in. Maybe increasing the provided PEEP and lowering the FiO2 somewhat before giving surfactant will help with distribution and increase your chances of first being able to extubate and secondly when you do keeping the tube out!
  6. 2 points
    https://www.frontiersin.org/articles/10.3389/fped.2018.00088/full https://www.frontiersin.org/articles/10.3389/fped.2018.00086/full https://www.frontiersin.org/articles/10.3389/fped.2018.00084/full And one more fascinating article on cardiovascular supportive therapies for the neonates with asphyxia: https://www.frontiersin.org/articles/10.3389/fped.2018.00363/full fped-06-00363.pdf
  7. 2 points
    These are brilliant! Sent from my iPhone using Tapatalk
  8. 2 points
    I recently had the honour of being asked to present grand rounds at the University of Manitoba. My former Department Head during the question period stumped me when he asked me what role angiotensin converting enzyme 2 receptor (ACE2) has in pediatric COVID19. Like all great teachers, after I floundered and had to confess that while I was aware there is a role in COVID19 I wasn’t sure of the answer, he sent me a paper on the subject. The reality is that a very small percentage of COVID19 illness is found in children. Some estimates have it at 2%. Why might that be? It’s what’s in the nose that matters What has been known for some time know is that the point of entry for SARS-CoV-2 is the nasal epithelium. What is also known is that the receptor that the virus binds to in order to gain access to the host. Such binding and what happens after the virus gains entry to the body is shown in this figure depicting the life cycle of SARS-CoV-2. In a research letter by Bunyavanich et al Nasal Gene Expression of Angiotensin-Converting Enzyme 2 in Children and Adults looked at 305 patients from ages 4-60 years to examine biomarkers of asthma. In the course of looking at the nasal epithelium of these patients, they found age related differences in the expression of ACE2 receptors as shown in the following figure. I think the results somewhat speak for themselves. The younger you are the less receptors you have. If you have less receptors maybe you are less likely to contract the virus! What we don’t know This research leads to some interesting questions. Drugs such as losartan and valsartan already exist and function by blocking he ACE2 receptor. Could blockade help to limit the spread of infection? I am not aware of any such trials going on at the moment but something worth looking at. The other point that needs to be raised is that the most vulnerable group of ages >60 were not looked at in this study. The trend would certainly indicate that with age we would expect the receptor numbers to increase but since we don’t actually have the data in the older groups we don’t know if receptor numbers start to fall again with age. Similarly we don’t know below the age of 4 what receptor numbers are like. In examining risk of vertical transmission it is worth noting that the recent placental positive RT-PCRs as in Detection of SARS-COV-2 in Placental and Fetal Membrane Samples. In that study while 3 of 11 placental membranes tested positive, none of the newborns were infected. Could it be the fetus and newborn is protected by having very little density of ACE2 receptors? Something to look at and will be no doubt. Regardless, in the fight against COVID19 maybe one direction for therapeutic targeting should be addressing this receptor and seeing if there is something we can’t do to make it less susceptible to binding.
  9. 1 point
    @K. S. Gautham Thanks for sharing! @all - here's the direct link to the paper by Patil et al: https://www.nature.com/articles/s41372-020-0765-3
  10. 1 point
    I understand that it may be a long time ago you had issues w this baby but I would point out couple of things. Hope you weathered the storm and baby survived. It appeared that from the beginning baby had poor chance. It is important to have good recruitment of the lung before you give surfactant. You dont want it to go only to opened alveoli as the ones closed will be very stiff and eventually end up w PIEs. Undoubtedly Jet is superior to HFOV for PIEs. Jet doesn’t ventilate PIE alveoli allowing them to heal. Ask Dr. Keszler for advices when in question. Next, when you cant oxygenate, like last few CXR shown, and kid is hyperexpanded you are decreasing preload and at the same time obstructing pulmonary flow. You have to drop MAP on HFOV. You need to learn POCUS to look at the heart filling while managing tough cases like this. Also lung US helps a lot. Read Australian and McNamara studies on POC ECHO as well as Kurepa et al. paper on lung US. Finally using higher or lower Hz depends on each baby. See what works for your kid. Remember CXR is just one quick shot in time. All the best.
  11. 1 point
    POCUSNEO Canada is pleased to announce the first e-workshops in advanced hemodynamics starting from 1️⃣5️⃣ August 2️⃣0️⃣2️⃣0️⃣ https://pocusneo.org/e-workshops/ https://pocusneo.org/e-conferences/ Yasser Elsayed (University of Manitoba) Muzafar Gani (McMaster University) Emailing E-conference Flyer final R.pdf
  12. 1 point
    My pleasure. Couldn't resist to share three of my most favourite articles on the same topic from Frontiers in Pediatrics. Might-be of your interest. fped-06-00088.pdf fped-06-00086.pdf fped-06-00084.pdf
  13. 1 point
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