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Showing content with the highest reputation since 12/19/2019 in all areas

  1. 2 points
    First off I should let you know that we do not do transpyloric feeding for our infants with BPD. Having said that I am aware of some units that do. I suspect the approach is a bit polarizing. A recent survey I posted to twitter revealed the following findings: I think the data from this small poll reveal that while there is a bias towards NG feeds, there is no universal approach (as with many things in NICU). Conceptually, units that are using transpyloric feeds would do so based on a belief that bypassing the stomach would lead to less reflux and risk of aspiration. The question though is whether this really works or not. New N of 1 Trial I don’t think I have talked about N of 1 trials before on this site. The trials in essence allow one patient to serve as a study unto themselves by randomizing treatments over time for the single patient. By exposing the patient to alternating treatments such as nasogastric or nasoduodenal feedings one can look at an outcome and get a sense of causality if a negative or positive outcome occurs during one of the periods consistently. That is what was done in the study Individualising care in severe bronchopulmonary dysplasia: a series of N-of-1 trials comparing transpyloric and gastric feeding by Jensen E et al from the Children’s Hospital of Philadelphia. The authors in this study determined that using a primary outcome of frequency of daily intermittent hypoxaemic events (SpO2 ≤80% lasting 10–180 s) they would need 15 patients undergoing N of 1 trials between nasogastric and nasoduodenal feeding. Included infants were born at <32 weeks and were getting positive airway pressure and full enteral nutrition at 36 0/7 to 55 6/7 weeks PMA. Infants who were felt to be demonstrating signs of reflux or frank regurgitation were enrolled. The findings Thirteen of 15 enrolled patients completed the study. The two who did not complete did so as their oxygen requirements increased shortly after starting the trial and the clinical team removed them and chose their preferred route of feeding. Randomization looked like this: Of the 13 though that completed and using an intention to treat analysis of the other two the findings were somewhat surprising. Contrary to what one might have thought that transpyloric would be a lung protective strategy, the findings were opposite. Overall the combined results from these 15 patients demonstrated that nasogastric feedings were protective from having intermittent hypoxic events. How can this be explained? To be honest I don’t really know but it is always fun to speculate. I can’t help but wonder if the lack of milk in the stomach led to an inability to neutralize the stomach pH. Perhaps distension has nothing to do with reflux and those with BPD who have respiratory distress with some degree of hyperinflation simply are prone to refluxing acid contents due to a change in the relationship of the diaphragmatic cura? It could simply be that while the volume in the stomach is less, what is being refluxed is of a higher acidity and leads to more bronchospasm and hypoxemic events. What seems to be clear even with this small study is that there really is no evidence from this prospective trial that transpyloric feeding is better than nasogastric. Given the size of the study it is always worth having some degree of caution before embracing wholeheartedly these findings. No doubt someone will argue that a larger study is needed to confirm these findings. In the meantime for those who are routinely using the transpyloric route I believe what this study does at the very least is give reason to pause and consider what evidence you have to really support the practice of using that route.
  2. 2 points
    I have observed this repeatedly in babies whose mothers were taking SSRI antidepressants, specifically Zoloft. Happy baby who does not cry. Cheers, MK
  3. 1 point
    Thanks! Without you and all other members, there would be no community!
  4. 1 point
    I cannot access the full text from home, but it strikes me that intermittent hypoxia is, at best, a surrogate for the clinical indication I and my colleagues have done trials of post-pyloric feeding in this patient population. As you say, practices vary, so perhaps I'm an outlier, but I use post-pyloric feeding for the very specific subpopulation of BPD patients for whom I am trying to modulate the mode of support (eg wean the baby who is 'stuck' on a low level of CPAP or a HFNC from positive pressure to a low flow canula that can be weaned on an outpatient basis). These trials of post-pyloric feeding typically run ~1 - 2 weeks and the outcomes we follow are (in order from least to most important): intermittent hypoxemia, baseline FiO2 changes, changes in level of support. I agree that those who seldom or never resort to transpyloric feedings need not change their practice based on this study, but I'm not sure this trial addresses the way transpyloric feeding is used in my part of the world.
  5. 1 point
  6. 1 point
    Dear collagues In our nursery we use BabyFlow from Dräger to provide NIV via VN500. We are planning to introduce the Seattle-PAP system (a bubble CPAP system) from Dräger to deliver nCPAP. Previously we have used beneveniste-CPAP. So moving to BabyFlow is quite a big step as the headgear and interface is quite different and much more bulky compared to what we have used for many years. Is there anyone out there using BabyFlow who would be willing to share experience? Our nurses are working hard to get used to the nasal interface and fixation system and especially when using bubbleCPAP we have lots of difficulties with leakage. many thanks in advance cheers Christian A few words about the unit: Level 3 NICU in Denmark. From 23 weeks GA to term+, noninvasive resp support and Conventional and HFO ventilation, iNO, ECMO, cardiac and pediatric surgery on site in addition to ENT, ortho and neurosurgical surgery and retrieval service
  7. 1 point
  8. 1 point
    I find this web and app resource from Cincinnati Hospital extremely useful to teach students/ trainees and during parent consultations to explain the condition in 3D (saves me the embarrassment from drawing!) Weblink Link to play store to download the Android version.
  9. 1 point
    A colleague of mine has one such probe and said she would let me try it ( after New years). Will report back!
  10. 1 point
    Have a case: Stat CS for maternal abruption and decels Term baby. Poor tone and resp effort. Suspected blood aspiration. Needed PPV and 100% FiO2 for hypoxia. Intubated in DR. Cord gases pH 7.22 BE -8 Baby H/H: 18/50 Baby gas 7.18 / -8 at ~50 min of life Started having clinical seizures at 12 HOL. Electrical seizures on EEG. Normal HUS. Would you start late therapeutic hypothermia? Did not meet mod/severe sarnat encephalopathy on exam but was hypotonic, was intubated, and required prolonged resuscitation. TH is often fairly well tolerated and there's not much else to do. 2017 Laptook paper suggests potential benefit with late cooling. The baby had a perinatal event and clinical signs of possible HIE but no acidosis. Could be stroke or other. Some papers looking retrospectively at cooled infants who went on to have perinatal stroke had seizure reduction with TH. So far has received phenobarb, keppra, fospheny for refractory seizures.
  11. 1 point
    I think it's fairly reasonable to attribute the baby's seizures at 12 hours to an etiology other than HIE. The cord gas is ok and also the gas at 1 hour can be attributed to the resuscitation YES. But it could be also respiratory as you have not mentioned the PCo2. And again regarding the gas at 1 hour of life... It's not that acidotic to start cooling ( Looking at the CPS statement of 7.15) I think guidelines are made for those situations ...to help when things get blurry. Sticking to it as is the right thing for me until an alternative approach has established evidence behind it.
  12. 1 point
  13. 1 point
    A male baby normal vaginal Delivery cried spontaneously with satisfactory Apgar, 1,5 and 10 minutes. Mother didn't receive any narcotics at delivery.history of rupture membrane 24 hours before delivery. Amniotic fluid is clear. Baby has good color but no cry. what you think?
  14. 1 point
    Great question, Juan Carlos. I am partial to the VN500, but I'm sure both devices can deliver VG quite well. The problem is that babies don't like to be acidotic. Consequently, there is a problem with permissive hypercapnea in the first days of life in small preemies, because their kidneys are not able to compensate for respiratory acidosis. Therefore, the baby will try to generate a tidal volume sufficient to bring the PCO2 down and normalize the pH. As you know when the tidal volume exceeds the target value, PIP will come down and pretty soon, your baby may be on endotracheal CPAP with rising oxygen requirement (due to the drop in MAP), tachypnea and increased work of breathing. You would have to sedate the baby sufficiently to suppress their respiratory drive, which is a bad idea. People find all kinds of ways to reduce the support for the baby's effort, for example changing from AC to SIMV at a low rate, so the baby is unable to generate adequate minute ventilation and correct the acidosis. So, the baby is struggling, but the doctor is happy, because the PCO2 is where he or she wants it. If you can buffer the acidosis by adding some acetate to your TPN and get the pH up to near normal, you might be able to let the CO2 rise gradually. The focus needs to be on pH, not PCO2, because it's the pH that is the primary stimulus for respiratory drive. Basically it is better to support the baby's effort to maintain normal pH and avoid the mistake of looking only at the PCO2. Ultimately, it is the perivascular pH that controls cerebral circulation, but unfortunately all studies keep focusing on PCO2 and ignoring pH. What we know is that rapid fluctuations in PCO2 confer the greatest risk of IVH. Once the baby is a bit older and the kidneys are more mature, it'a s lot easier to allow permissive hypercapnia if they still need mechanical ventilation. I hope this helps, MK
  15. 1 point
    This would be my take - if the infant seems perfectly well, I would not worry too much. On the other hand, if there are some minor clinical signs/symtom (like some reduction in muscle tone, not perfectly normal feeding behaviour etc-etc), I'd be suspicious and probably do some basic lab workup and then refer for clinical followup with the community pediatrician (and then he/she refers back in case of increased suspicion of congenital disease)
  16. 1 point
    Dose & administration Three doses at 24-hour intervals, as intravenous injections over 15 minutes, or by oro-gastric administration: 1st dose: 10 mg/kg 2nd and 3rd dose: 5 mg/kg Indications Closure of the patent ductus arteriosus. Contraindications and special considerations (incl incompatibilities) Contraindications include: duct-dependent cardiovascular malformation active bleeding, including intracranial, gastrointestinal or lung bleeding necrotizing enterocolitis (confirmed or suspected) significant thrombocytopenia or coagulation defects significantly reduced renal function significant hyperbilirubinemia Pulmonary hypertension has been reported when ibuprofen was given within 6 hours after birth. Concomitant use the following pharmaceuticals products is not recommended: diuretics: ibuprofen may reduce the effect of diuretics, and diuretics may increase the risk of renal insufficiency in dehydrated patients. anticoagulants: ibuprofen may inhibit platelet function and concomitant use with anticoagulants may increase the risk of bleeding corticosteroids: concomitant use with ibuprofen may increase the risk of gastrointestinal bleeding nitric oxide: since both nitric oxide and ibuprofen inhibit platelet function, concomitant use may in theory increase the risk of bleeding other NSAIDs: concomitant use of more than one NSAID should be avoided because of the increased risk of adverse reactions aminoglycosides: ibuprofen may reduce clearance of aminoglycosides, concomitant use may increase the risk of nephrotoxicity and ototoxicity, and surveillance of serum levels of aminoglycides should be performed Ibuprofen should not be administrated with any acidic solution. Adverse effects Oligura and transient renal insufficiency. Ibuprofen has less renal side-effects than indomethacin. Pharmacological aspects Ibuprofen is an anti-inflammatory drug (NSAID) that reduces the synthesis of prostaglandins through a non-selective inhibition of cyclo-oxygenase. Prostaglandins are involved in the persistence of the ductus arteriosus after birth, through relaxation of the muscle layer of the ductus arteriosus. The reduction of prostaglandins by ibuprofen is believed to be the main mechanism of action. The estimated T1/2 is 30 (16-43) hours. References Summary of product characteristics. Pedea -EMEA/H/C/000549 -IG/392. (URL) Ibuprofen for the treatment of patent ductus arteriosus in preterm or low birth weight infants. Cochrane Database of Systematic Reviews 2015, Issue 2. Art. No.: CD003481. 
PMID: 25692606 Pulmonary hypertension after ibuprofen prophylaxis in very preterm infants. Lancet 2002; 359: 1486–88. PMID: 11988250 Document version history 2017-02-10 / Stefan Johansson
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