abeluchin

It is my pleasure to inform the group that I successfully passed the neonatal-perinatal board exam. It was a very difficult test. I wanted to thank all the support given here . The references suggested and the frequent cases and discussions posted here made a huge difference. THANKS 99NICU!!!!

Thanks for the feedback. There are some publications that bring concerns about the increased incidence non-GBS sepsis, particularly e'coli in premature infants after implementation of GBS guidelines. Some of my colleagues are concern that we may be ignoring this possibility by implementing the new guidelines which is focus on GBS only. Another argument is that the guideline does not address the more preterm and susceptible baby and we might be waiting until it could be too late to intervene. What's your take of these points? Thanks

A question for the group. This new guideline apply to every gestational age. I just came up with a of a set twins that were born prematurely at 32+ weeks. Mother GBS status was unknown, babies were delivered by c-section due to breech presentation in one of them. ROM was at delivery. Both babies were born vigorous and transition without issues. The continued asymptomatic at a week of life. I decided to consider the recommendations of the 2010 GBS guidelines and did not start them on antibiotics. A CBC was reassuring and BCx was negative at 48hrs. Before the 2010 guideline, I would start any 34weeks or < preterm asymptomatic baby on antibiotics if the reason for preterm delivered was other than maternal due to the high association of preterm labor and sepsis. 1. What are you doing in your practice? 2. Are we missing an important window to prevent early-onset GBS or non-GBS sepsis in the most preterm and vulnerable baby? 3. Are we overusing antibiotics in this population? or this is not a big deal for most of us? Thanks for any feedback on this!!

Thanks Dr. Sanghvi for you input. In my practice, when I go from a pressure-limited mode such as AC or SIMV to a volume-target mode such as volume guarantee in the Babylog 8000+, I looked at the previous 15 to 10 minutes average tidal volume and set my target volume around that one, usually keeping it in the physiologic range of 4-6ml/kg. I do not generally see an increase in driving PIP to deliver that set volume. I would assume if your tidal volume is set blindly at 5/kg, your driving pressure could be higher or lower than in your pressure mode, depending on the lung compliance and airway resistance. Again, I think that based on most recent publications VG mode is associated with less biotrauma that pressure modes, giving that you control the most important variable associated with VILI (VOLUME). THANKS

http://www2.aap.org/nrp/

We are taught in fellowship and by many publications that barotrauma is a factor for VILI in neonates. As a general rule, I use many pointers in management of a ELBW infant during mehanical ventilation to prevent VILI, inluding optimizing lung volume, volume-target ventilation and permissive hypercapnea. I use HFOV as a rescue option when pt develop worsening respiratory acidosis despite implementing the criteria above, or worsening lung compliance as indicated by requiring increase driving pressure on the vent to meet target tidal volumes. I also use the HFOV in air leak syndrome, pulmonary hypoplasia with pulmonary hypertension, among other indications. I do not generally use HFOV as a primary vent in small preemies, but some centers do. My question to you is: initial settings on CMV (with PIP over 25) in babies < 1kg during volume-target ventilation are generally accepted as too high and potentially a cause for barotrauma. One caviat to this general rule is that during volume-target ventilation, TV is control and barotrauma plays a less important role in development of VILI. Another point is that when a 2.5 ETT is used to ventilate a 800g baby or smaller the resistance of the airway increases signicantly and babies usually require higher driving pressure to overcome this resistance and meet the target tidal volume. These small ETT are usually easily obstructed by mucus plugs in the airway making the resistance to increase even further. Base on the above assumptions, I do not generally switched babies with small ETT 2.5mm, from volume-target CMV to HFOV to follow the principle of gentler ventilation when the PIP is high or increasing, unless I see obvious deterioration in compliance associated with a inter-current condition such as PDA or sepsis. In fact, I do tend to ignore the PIP when a small ETT (2.5mm) is used as long as I am able to achieve sustained lung inflation without secondary respiratory acidosis or hypoxia, and of course I cannot replace the ETT to a bigger or fresher one. How do you approach this problem on your daily practice? Thanks

How do you differentiate PIE vs. early cystic BPD? A former 25week preemie developed cystic lung lesions as evidence of chest x-rays at 2weeks of age. The infant was born through maternal chorio, no NAS given, developed RDS, required two doses of survanta and antibiotics started for suspected sepsis, completed 7 days. Initial Hct was 19, infant received multiple PRBS transfusions, but developed pressor-resistant hypotension requiring Dopa/Dobutamine/Epinephrine/Hydrocortisone. A left grade 4 IVH and right grade IVH was noted on DOL2, stable on follow ups. Pt remained on CMV, moderate settings until DOL7 that was switched to HFOC due to requiring significant peak pressures on CMV and higher FiO2 requirments. A BCx was repeated(grew staph epi) and broad-spectrum antibiotics started (vancomycin and gentamicin). A repeat ECHO showed a large PDA with left-right shunt and left atrial enlargement. Pt was treated with Indomethacine with resolution of the PDA. DOL7-10, Pt developed hypotension requiring dopamine and hydrocortisone, and worsening lung compliance requiring higher means on HFOV to maintain lung inflation. FiO2 requirement was 80 to 100% throughout. Amphotericin B was added in the mist of the set-back to due concerns with fungal infection. On DOL12 lungs were noted hyperexpanded, unable to wean mean airway pressure due to profound desaturations wih every attempt. Pt on heavy sedation and paralysis at this point. On DOL13 bubbly lucencies were noted on x-ray. No pneumothorax seen. 1. My best guess is that this is stage 3 of the old BPD, given late presentation of the bubbly lusencies, non-association with pneumothorax or other air leak problems and very strong predisposition to severe BPD, such as ELGA, maternal chorio, no ANS, PDA, sepsis and mechanical ventilation. 2. PIE is a probably diagnosis, but I've seen PIE presenting earlier (particularly in the first 1-2 days of life), almost always associated with pneumothorax, in babies with hypoplastic lungs, mec aspiration or uneven surfactant distribution and severe RDS. I do not think we can differentiate radiologically PIE from early cystic BPD, so that we cannot make a radiologic distinction between SIP and early NEC with perforation. I would like to hear your opinions on how you differentiate these two entities in clinical practice? Do you usually make a distinction between the two? or you think they are a continuous of the same disease process? Thanks in advance for you inputs

I would love to see the pics. If you could send them in a compressed file to abelg66@hotmail.com Thanks

this is still a grey area in NRP, even in the 6th edition. The evidence does not show that tracheal suctioning in mec-stained amniotic fluid babies prevent mec aspiration, but "Absence of evidence does not equal evidence of absence". We know that most mec aspiration occurs in utero, and only small percentage can occur shorty after birth, and tracheal suctioning does not prevent the aspiration that has already occur, but may it could prevent a small percentage of aspration that can occur after birth, or at least eliminate the blocking mec articles sitting in the airway from in-utero aspiration, so that ventilation is achieve easier Based on this assumptions, I agree with Dr. Stefan that not all babies born through mec-stained amniotic fluid need tracheal suctioning (and a neonatologist present) just the ones that may have aspirated in-utero due to gasping breaths (Those with NRFHTs). The competence of the labor and delivery responder should of course be a factor, but this is a standard NRP recc that one person able to initiate NRP (Able to stim, warm, suction and bag if needed) should be present at every delivery, this allow the Neos to be available within a reasonable time to respond if the infant needs intubation. In our institution we have stablished: 1. Vigorous babies born through mec, regular NRP is provided 2. Depressed infants born through light mec, regular NRP, if apnea persists ppv is provided 3. Depressed infants born through thick mec with no h/o NRFHTs, (likely terminal mec), regular NRP plus oropharyngeal suctioning, and ppv if apnea persists 4. Depressed infants born through mec with h/o NRFHTs, tracheal suctioning followed by regular NRP, ppv if bradycardia develops.

Thanks all of you for the good advice. Dr. Feraszaman, would you please clarify your comment about the study Pdf Mcq from 80's? How can I get this reference? Thanks

Thanks for the feedback Stephan. I did place the leg in comfortable semi-elevated position and the swelling went away Cheers

Yes, I meant the three above (Rule Out Sepsis with the abbreviation(ROS), IntraPartum Antibiotic with (IPA) & Group B Streptococcus with with (GBS). Sorry for using these abreviations

I've been managing a term severe IUGR infant of 760g for the past two days and noticed recently that the lleg where a PICC line was placed the night before is slightly swollen. Unfortunately a 24gauge PICC was inserted. The leg is swollen mainly from the knee down to the foot unilateral, with only slight compacticity in the isolateral thigh, with no redness or increased temp. The opinion of the PICC team is that this is cause by obstruction of the venous flow and close monitoring should be suficient for now. I am concerned about the development of DVT! 1- Have you seen this associated edema in an extemity with a PICC line due to vein flow stasis? 1- Will you monitor these babies clinically without pulling the PICC out if no worsenng, severe or associated with compromised perfussion? Thanks for your experinced advice

I would like to hear your opinions in regard to starting antibiotics for ROS in preterm asymptomatic infants born due to reasons other than purely maternal (such as c-section for NRFHT, Premature ROM with preterm labor)? 1- Any GA cut off? 2. Based on GBS status and IPA prophylaxis adequacy? Thanks for your response

Hi, I will be taking the certifying exam for neonatal-perinatal medicine next March. Unfortunately, I will not be able to attend any review course due my current practice location. I would like to get you opinion in materials, books, online reference to study for the board? I would be great if I cold access somebody subscription to the last neo-Conference for neonatology (from pediatrix), or the questions (I am willing to pay for it). Thanks

On VLBW/ELBW preemies with mild residual RDS, stable on NCPAP with FiO2<30% we wean by 1 LPM every 2-3 days until off.

" Do you have a certain formula to calculate the mmol/ kg/ day of a Sodium or Potassium infusions?" I think she is asking how to calculate the moles of Na or K in different solutions that are used to prepare the TPNs.

I was would like to know what most practice in regard to timing of inguinal hernia repair on preemies. I have found this question sometimes difficult to answer given the magnitude of implications which I would like to mention and get your opinion on: 1- Preemies are at higher risk to develop acute surgical complications from a inguinal hernia compared to older infants, but I've never seen one occur in over 7 years of NICU experience, have you? 2- Some consider the repair of an inguinal hernia a relative surgical emergency because of the above, do you? 3- Most inguinal hernias in preemies will be repaired before the infant is discharge home from the NICU, do you do this? 4- Most inguinal hernia repair in preemies will require elective intubation and general anesthesia, but local anesthesia with mild sedation is possible, what do you do on your unit? 5- A large number of preemies with inguinal hernia also has CLD and intubating them for a preventive surgery seems to be inappropriate given a possible major respiratory set back, so waiting for 6 months to a year before repair seems reasonable, what do you think about this? Thanks

1- Are anybody out there using neobars to secure the ETT? 2- If you use neobars, explain why you prefer them over the adhesive tapes attached to the lip to secure the ETT 3- If you do not use the neobars explain why not. 4. Do you use any other method to secure your ETT? I do not want to skew your answers, so I will give my personal opinion later. Thanks so much for your participation in this short survey, any response will be greatly appreciated.

Thanks to all for your responses. It was indeed a very difficult case. I am as a young neonatologist trying to get the best experience from these difficult cases, and give the best possible care to the next baby in a similar situation Thanks again for your comments

Hi, I recently heard of a case of an infant born at term from an apparently uncomplicated pregnancy. Mother of the infant with h/o sickle cell trait. Mother visited the OB doctor at 40 weeks due to painful contractions. Questionable decreased fetal movements was recollected on further questioning, but no clear on initial presentation. Mother was admitted to L&D due to active labor. A stat c-section was performed after 4hrs of labor due to a category III fetal heart tracing (with absence of variality). A severely depressed infant was born through meconium-stained amniotic fluid. ET intubation was performed, but no mec was seen below the glottis. PPV was initiated due to persistent apnea and neonatologist was called. Infant was immediately intubated and transported to the NICU while been bagged at 25/5, 100% FiO2. Upon admission to the NICU, a stat ABG was performed that showed severe metabolic acidosis (7.0/73/25/-20) and severe anemia with a HCT of 19. O2 sats in the low to mid 50's. HR always above 100. Infant was placed on HFOV and umbilical lines placed. A NS bolus of 10ml/kg was given (3.3kg weight) and PRBC was requested stat. Infant oxygenation failed to improve, with O2 sats now at 0. A trial of CMV was attempted with some improvement in O2sats. F/U ABG with worseing metabolic acidosis (ph 6.5,BE -30), but PCO2 in the low 40's. CRX with clear lungs and normal CTS. Infant in shock, received 2 additional boluses of NS at 10ml/kg, and finally PRBC at 1 HOL, with IV transfusions over 10 minutes each. Infant was started on dopamine, dobutamine, epi for persistent hypotension with shock. ECHO with poor bi-ventricular dysfunction and PPHN, normal otherwise. iNO started. Infant did not show improvement in oxygenation, and after several rounds of chest compressions for severe bradycardia, withdrawal of care was suggested and infant died at 4 HOL. Questions: 1. Have you managed this infant differently? 2. The primary cause of the shock and hypoxemic respiratory failure was speculated to be the severe chronic anemia(given aneia with large amount of PRBC and evidence of hemolysis on peripheral smear), but we have all see infant with worse anemia that are way more stable on initial presentation 3. Have you chose to exchange transfusion instead of direct PRBC transfusion, despite the poor initial presentation with severe anemia, with anemic shock and severe hypoxemic respiratory failure? 4. In your personal practice, what patient with chronic in-utero anemia do you transfuse vs. exhange transfusion at birth? Thanks for any comments

Thanks to all for your responses.

We are trying to put together a nurse NRP response team to cover neonatal L&D emergencies until the neonatologist arrive at the scene. My specific questions are: 1. Can you legally train nurses to be the immediately available person capable of performing a full neonatal resuscitation, including, PPV, intubation, chest compression, and UVC epi/volume administration? 2. What is your experience in the legal burden (for the nurse and the neonatologist) of this practice? 3. In small non-tertiary hospital, what is the usual required response time for the on-call neonatologist to attend L&D emergencies? Thanks so much

Dear Ibrahim, Thanks for posting this interesting question that may be beneficial for discussion in this forum. Superficial Thrombophlebitis is a known complication of venous access, which could be traumatic and or infectious.The main treatment of this condition is to remove the cause that predisposed its appearance, particularly removing the PICC or any hardware placed in the vein (angiocath), and treat with antibioticsif evidence of active infection (low thershold for antistaph coverage). A potential complication of superficial phlebitis is extension of the thrombosis to the deep venous system, with possible complicated with PE.I am not quite sure if application of warm compress will significantly help with the local swelling, and my concwern is that given the increased in heat production locally with the vein inflamation, warm compress may potentially burn the skin locally. I hope this help Bst wishes

NRBC count was low < 10%