abeluchin

It’s a very interesting study. Thanks for sharing it!

Hi there seem to be enough evidence about the lack of beneficial effect of treatment of the PDA! The approach to a hemodinámica significant ductus has changed significantly in the last 10 years. Years ago we weee so obsessed that indocin prophylaxis was standard in many NICUs and early treatment became standard across the board. I remember going to Dr Clayman PDA lecture at PAS where the PDA was seen as a demon many babies had been exposed to surgical ligation with a known consecuentes of a surgery on a small premie baby since William Benitez published his meta analysis about PDA there has been a definitive change in some centers on how to approach it and some has gone away from early treatment and surgery there are other centers that continue to ignore the Trent and treat the PDA like we used to 10 years ago. we I have noted in my practice is that regardless of the PDA size; baby that are on Mechanical ventilation after 7-10 days we give a course of tapering Decadeon (DATRT) and they get extubated i Belice fluid/sedation/lung protective strategy and steroids when use appropriately will result in better outcomes for our micro premie of 22-26 weeks whats are you doing in your practice? thanks

No other antibodies were present in mother's circulation.

Hi I took care of a baby who's mother is B+ and baby is A+ with a DAST/Coombs+. The DAT was sent inarventently since we only sent DAT in mother's with blood tupe O or rh negative. I was surprised to see this results since I have always understand that ABO incompatibility that cause significant hemolysis is only produced when mother is O and baby is A or B group. The reason for this ABO incompatibility set is not too clear. I understand its because when mama is O and baby is A or B; IgG antibodies casn be produced during gestation that will cross the placentas . Unlike when mama is A and baby is B or mama is B and baby is A only igM antibodies are produce yhjat will not cross the placenta. I am not sure why this is produced this way?? Any input or insights will be apreciated

Hi Johan; thanks for your insight. That’s the reality of my hospital. The anti lactation has taken this unpublished recommendation to prevent mother to lactate their infants

Hi group; our OB colleagues use Methergine (ergonovine) for treatment or prophylaxis of postpartum hemorrhage. The medication label from the manufacturer recommends to hold breast feeding up to 12 hours after last dose due to unpublished reported side effects in the babies i did a literature search and found only one article published in Pubmed that covers that topic: https://pubmed.ncbi.nlm.nih.gov/27846760/ min this prospective study they found no side effects in breastfed babies Are there any other reference on this topic that you can share? is this something that affects your newborn nursery practice in your hospital? Thanks for any input

Baby went home a couple of days ago. Wbc count at the lowest 26k and platelet count persistently above 120k

46 days old; former 28 weeker premature baby with persistent leukocytosis for over four weeks now. Uncomplicated NICU course so far. Since about the second week of life, the baby has had persistent leukocytosis with wbc count in the low to high 30k's. Baby has had multiple crp done and all normals. Culture from blood and Urine including fungal normal as well. Had a course of Meropenem for suspected UTI with 10k colonies of enterococcus fecalis in the urine; but despite negative repeat urine culture and after treatment; leukocytosis persisted. About two weeks ago; now baby with mild thrombocytopenia 80-90k. Cardiac echo done, renal and abdominal US all normal. Viral culture, RPR and urine CMV all negative as well. Currently baby is on room air; growing great. Feeding great. Had completed a 7 days with Fluconazole; without any improvement Hem consulted. Requested a flow cytometry; with left sided neutrophilia with 4% blast. Bone marrow not entertained at this point! What do you think? Anything comes to mind? Thanks

Hi colleagues, In the past few years the assessment of growth in the newborn has been updated significantly. In the US, we use Fenton for preterm < 35weeks, CDC and WHO for late-preterm and term babies. I have . WHO for uses growth charts for 0-24 months and does not consider GA at birth, , so babies could easily be over-classified by SGA, or LGA if GA at birth is not used. For example: using medcal interactive growth charts (CDC-based); a newly born male at 37weeks who weight 2600grams is classify as AGA between 25th and 50th%tile. A baby with same BW, but with a GA at birth of 41 weeks (term) will be considered SGA (<10t%tile) with medcal. but AGA based on WHO; since they do not stratify babies by GA. 1- what is your current practice to classify preterm or term babies based on BW? 2- what growth charts are you using? Thank you for any imput, references will be greatly appreciated

Thanks

I just had a LGA term baby born through shoulder dystocia; noted with respiratory distress shortly after birth. Placed on HFNC, need ~35% FiO2 on 2 LPM. Xray with right hemidiapragm elevation. Question: How long is prudent to wait for surgical intervention in these babies? Thanks

Thanks to you all for your response. The baby was transfered for neuro eval and expectant management was carried out.

Dr. Vijayashankara, would you please, explain a bit more why your practice was change from multiple to a single dose of surfactant? Thanks

It has recently been brought to my attention that the suture of the pedunculated vestigial digit in post-axial polydactilly has been associated with development of painful neuroma over time! I have always ligated these vestigial non-bonny digits and have them follow up with their PCP.Here is some of the articles: Pediatr Dermatol. 2010 Jan-Feb;27(1):39-42. doi: 10.1111/j.1525-1470.2009.01071.x. A selective approach to treatment of ulnar polydactyly: preventing painful neuroma and incomplete excision. Mullick S1, Borschel GH. Pediatr Dermatol. 2009 Jan-Feb;26(1):100-2. doi: 10.1111/j.1525-1470.2008.00835.x. Traumatic amputation of a supernumerary digit: a 16-year-old boy's perspective of suture ligation. Hartzell TL1, Taylor H. Pediatr Dermatol. 2003 Mar-Apr;20(2):108-12. Surgical excision of pedunculated supernumerary digits prevents traumatic amputation neuromas. Leber GE1, Gosain AK. what's your personal experience in this topic? Thanks

Hi, I recently care of a couple of 34 weeks Mono-Di twin male infants, one of them with a Hct of 37% and the other 47%. The BW was very similar in both twins at 1890g and 1900g and no h/o olygo was recorded in any of them. I ordered a retic count in the anemic boy, as well as a CUS and a KB test on the mother. KB test was reported as 0.15; with an estimated of fetal blood loss of 12ml. Retic count was 16% and came down nicely over three days to 8%. Hct remained stable in the low 30%. Both kids were asymptomatic since birth and are feeding and growing well. Questions: is this presentation consistent with significant Feto-Maternal Hemorrhage (FMH)? Can FMH affect preferentially one twin in Monochorionic twin pregnancies? Mother weight 83kg. I estimated 12ml of fetal blood loss based on the following calculations: maternal blood volume 70ml x weight in kg= 5810ml plus an increased in 40% of blood volume during pregnancy equals 8134ml. If 0.15% was fetal blood that equals 12.2ml of feto-placental blood loss. If feto-placental blood volume is ~100ml/kg of fetal weight, then 1.890 x100 is 198ml of total feto-placental blood, so 12.2ml represents <5% of the total feto-placental blood volume, which for me does not explain the reticulocytosis or anemia present in this infant, what's your opinion? thanks for any feedback!

What is your experience with this condition and performing frenotomy? Thanks

Thanks for your responses.

I would love to hear your local practice in regards to repeated doses of surfactant in neonates with respiratory distress? The study publish by Soll in cochrane showed benefits of multiple vs single dose, but the RCT were done in the 90's when gentle ventilation and antenatal steroids were not standard in the NICU! What do Neos across the world do in this regard? If you do repeat the treatment, what is your criteria? GA, time after birth, degree of respiratory distress or respiratory modality? Thanks for you feedback on this interesting topic. I am a neo neo trained in the post surfactant era, support trial and nCPAP to treat very small preemies with RDS, so is not hard for me to incorporate these new modalities in our practice! If you do not use repeated doses of surf, can you provide any reference that support this practice? Thanks

Hi colleagues, I had the pleasure recently to manage a premature infant (30wks EGA), who was born by precipitously vaginal delivery after mother arriving at the hospital with abdominal pain and vaginal bleeding, (later confirmed to be placental abruption). Good prenatal care, GBS positive in mother's urine 3wks PTD. The female infant was born lifeless, required PPV and chest compression by the bedside nurse and was intubated quickly when the neonatology arrived at the bedside at 2 MOL. Apgars 1,3 and 7. Infant was brought to the NICU placed on CMV initially at 20/5, then increased to 25/5, RR of 40, FiO2 40-60%; suvanta given and PIP pressures reduced slowly to 18/5. BP unreadable, very poor perfusion noted. BW 1.2kg.. UAC.UVC placed. Initial ABG 7.1/58/-12.5(not too bad). Infant had received 2NS boluses by the time I arrived. BP still with a mean in the low twenties and very poor skin perfusion at this point. Abx ordered and given stat. Initial Hct of 32%. PRBC ordered and given within 2HOL. After PRBC color improved and FiO2 was 30%, although BP was still low and a repeat ABG 7.2/53/PaO2 49/-5.1. Initial BS was also low and three glucose boluses given and GIR adjusted. Hydrocortisone one dose was given. An ECHO was ordered at this point and severe PPHN with suprasytemic pulmonary pressures was noted, normal cardiac function otherwise, large PDA bidirectional shunt. Infant was started on Dopamine at 10mcg/kg/min with titration to maintain systolic BP >50, up to 15mcg and dobutamine later added at 5 mcg with good response. PEEP was increased to 6 and FiO2 was increased to achieve a PaO2 in the 80 to 100. At this point, a blood culture was reposted positive for gram positive cocci in chain (later reported as GBS). Once BP was stable, fentanyl and versed were started PRN to keep the infant sedated and comfortable. A dose a NaBicarb was given later on with a -7.5 base deficit, which was infused over 2hrs(acidosis was felt to be related to urinary bicarb loss) and a Calcium run for a iCa of 0.8. Infant slowly improved and is now on 2 LPM of HHFNC at 21%, off vasopressors, repeat ECHO with no PPHN. Question: 1- Did this infant truly have PPHN? it is not uncommon to see mild transient elevated right ventricular pressures in premature infants with RDS, but this infant was clinically unstable and had three factors that could lead to malignant PPHN if untreated. I do understand the limitation of echocardiography in the diagnosis of PPNH, but given the risk factors and clinical presentation I felt and could not wait and see what happens. I would love to hear your personal experience in this type of patients in regard to diagnosis. 2- How different from the term infant do you manage premature infant with significant PPNH? I was trained to manage then equally, except for INO and <34wks, but I will still address the factors that aggravate PPHN such as hypoxemia, anemia, hypotension, hypoventilation, hypothermia, acidosis, agitation and hypocalcemia. 2- What is your experience with the use of sedation, paralysis in premature infant with PPHN? my practiced have been to avoid pain and agitation with PRN doses of fentanyl or Morphine and a benzodiazepine. I do not routinely use a fentanyl or verses drip or paralysis in my preemies with PPHN. 3- What about bicarb in PPHN?: Over the past few years, there have been a significant criticism to the use of bicarb in the NICU particularly in the acute setting with acidosis, but in the infant with PPHN, I still use it, particularly when I have achieve good perfusion, adequate ventilation and acidosis persists. My practice in this situation is to infuse bicarb very slowly over 2-4hrs and next day add acetate to the TPN Thanks for sharing your personal opinions in this topic best wishes respectfully Dr. Guerra

Hi colleagues, We use PICC in the NICU all the times and seldon have complications. There several emntioned complication from PICC lines, particularly the malpositioned ones. PICC lines at times, as you all know are critical in the management of preemies and it is very improtant to understand risk and benfits of keeping a line when it is placed. I recently seen a couple of radiology report requesting to remove PICC lines because project into the liver. I though understand that the hepatic vein are very difficult to catheterize with a PICC line (as opposed to umbilical catheter), especially once you have inserted a PICC and is sitting above the diaphragm, if you pull it back, it will be unlikely to retrograde enter in the hepatic veins. I trained to accept PICC as well placed when(those in the lower extremities), the tip lies in the IVC, no kink or bends and at least at or above L4-L5, this ways making sure you went beyong the lumbar veins (common entrance of lower extremity PICCs). Based on this: what is you practice regarding PICC tip placement? any with experience in PICC entering the liver? Any case report? Thanks

Hi coleagues, I recently came across to a baby in the newborn nursery with what appears clinically as a subgaleal hemorrage (SH). The infant was born at term 2800gram BW, required internal cephalic eversion x3, but no vaccum or forcepts were used. Initial exam was normal except for some scalp bruises. At ~ 8HOl, a significant scalp swelling was noted, concerning for SH( given the boggy sentation of palpation and that is covered all the occiput bilaterally), serial exam showed no significant progression of the swelling, and no extension into the neck. Head Circumsference initially was 33cm and did not increased on serial exams. Infant showed no ssx of shock, poor perfusion or CNS sings. Initial Hct was 55% and f/u Hct was 46% and remained stable with consecutive blood draws.Infant was feeding well in the NBN Infant was doing well, but another member of the staff decided to obtain a CT scan that showed a small pin-pong parietal fracture with sorounded soft tissure edema and questionable SH Based on this presentation: 1- Do you obtain brain image in every suspected SH? 2- Do you obtain brain image in clinically apparent SH in the abscent of neuro symptoms? 3- Do you ussually manage small SH in the newborn nursery until discharge home, if the baby remains clinically stable? Thanks

Lidocain?

Thanks. Any one depicting weight/HC by GA?

What charts for term infant are you using? Is it the most updated? Thanks

Hi there, I recently have a discussion with my colleagues about the risks involved in managing neonates with below the liver UVC and running TPN through it. I could not find case reports that enlighten a better science. I would like to hear your opinion about this topic. What is your practice? 1. do you use low-line UVC to administer TPN? have you ever had any liver injury from TPN extravasation? if you use TPN in low-line UVC, is there any osmolarity you feel safe with? what about Ca in the TPN, do you use it regularly on low-line UVC? Thanks your your responses v/r Dr. Guerra