HickOnACrick

As of yesterday, baby has continued to wean slowly on HFNC. FiO2 needs are mostly <40% on 3 LPM. Most importantly, baby has started bottle-feeding. We were very concerned about oral aversion. Baby remains on caffeine, multivitamin with iron, and Pulmicort NEB BID. Baby is gaining weight on a mixture of EBM and Neosure. When we have a baby that seems to be failing on HFNC, we generally move them over to NBCPAP or NIPPV, but we have used increased LPM flows (>5 LPM) on occasion. I have colleagues in other NICUs that prefer using HFNC at 6-8 LPM vs NBCPAP. We conducted surveillance PCRs on all staff that had a significant exposure to the family. We assigned the baby as a one-to-one nurse assignment so that nurse only cared for one baby. Baby has since come out of isolation. No other babies became symptomatic during this time, so no other babies have been tested for VRPs.

I use NaCl or NaAcetate in TPN. I can't remember the last time I used NaPO4. It is an option, but we do not use it often. We do not routinely check electrolytes until day 2-3, nor do we routinely add any supplements other than Ca and protein the first 2 days. What is happening with the weight of your babies that experience this hypernatremia? What about the urine output? A low UOP and substantial weight drop could imply lack if intravascular free water.

Here is our initial fluid management strategy: <750 grams = 120 mL/kg/day 750 - 1000 grams - 110 mL/kg/day 1001 - 1500 grams = 100 mL/kg/day We use 0.25 or 0.5 Normal saline in our UAC lines, running at 0.5-1 mL/hr. We do not routinely see hypernatremia in the first week, transient hyponatremia from immature renal function seems more common to us. Outside of the UAC fluids, our babies do not see Na in their maintenance fluids until 2-3 days of life. Hope this helps

We have had 4 confirmed subgaleal hemorrhages (SH) in the past couple of months. We have long suspected that many caputs have an element of SH, but avoid CT imaging due to the radiation and that identifying a SH will not change our management in most cases, if the baby is otherwise doing well. Of the 4 recent cases of SH, 2 have had more severe intracranial bleeding (intraventricular and subdural hemorrhages) and skull fractures - one of which was depressed. One of the cases was clearly in need of further head imaging on admission, due to the clinical picture, but the other was much more occult. This seems to be the crux of the problem - suspected occult subgaleal hemorrhage. Is imaging necessary to confirm? Each of these confirmed SHs had one thing in common - a drop in the Hct by at least 20%. The more severe cases experienced the drop earlier than the occult, less severe, SHs (12 hrs vs 48 hrs). Of the 4 cases, none required fluid resuscitation for hemorrhagic shock. With respect to the original questions: 1- Do you obtain brain image in every suspected SH? Not routinely. 2- Do you obtain brain image in clinically apparent SH in the abscent of neuro symptoms? I do now, especially if the Hct is dropping, or there is thrombocytopenia or coagulopathy. Skull radiographs may be enough to elicit a depressed skull fracture, which has possible implications in management. 3- Do you usually manage small SH in the newborn nursery until discharge home, if the baby remains clinically stable? Probably dependent on comfort level with your local nursery, but no, I would not feel comfortable if a known SH was in the nursery, unless the NICU had been consulted.

Going off service for a week, so an update. Baby has continued to slowly improve. Baby is now on HFNC 4LPM with oxygen needs around 30%, remains on full enteral feeds, fortified, and is gaining weight again. We may need to prolong the steroid course. As the course has weaned, baby's FiO2 needs have increased slightly (we have had the baby as low as 25% FiO2). The most recent chest radiograph shows improved expansion and aeration. Fibrosis and chronic changes are not the worst we have seen. We would not define the most recent CXR as being consistent with cystic BPD. We have spoken to a number of larger NICUs. This scenario (caretakers spreading C19 to NICU babies) is being seen in areas of the country where the incidence of C19(+) in the general population is the greatest. We have counseled our other families, especially those with the most fragile babies, that their social/work life needs to be a bubble of sorts.

I have found a few case reports about NICU graduates with BPD being admitted to PICUs with Covid-19. However, I have yet to find a case report of a former ELBW infant, who is still in the NICU, acquiring SARS-CoV-2, and deteriorating as a consequence. With regards to publishing, well, that is in part why I started this thread. It seemed like I was observing a novel effect of a novel virus, but wanted to see if others were seeing it as well. I reached out to my local University NICU's Medical Director, and they have not seen it in their NICUs. I have a couple other calls in to other large centers, but am awaiting their response(s). I plan to get IgG and IgM ELISA next week, considering whether it's worth testing mom's milk for virus and/or antibody. My local support for academic endeavors is greatly limited (county hospital), so I would welcome a collaboration if one has access to a more robust academic infrastructure. The baby's FiO2 needs are slightly higher today (35-40%). Work of breathing is better today, but baby remains dependent on the backup rate on NIPPV (currently set at 35 bpm). I have tested this daily by decreasing the rate at bedside. Baby continues to ride the rate and quickly desaturates if rate is weaned. A rate of 25 led to SpO2 of 70%. This, along with some increased irritability have me slightly concerned about neurologic sequelae. Thus far, his cranial ultrasounds have been clear - even for PVL. Baby is not receiving any sedation that would interfere with respiratory drive. The last blood gas was typical of a BPD baby - a mostly compensated respiratory acidosis - thus I believe the CO2 is available to drive respirations. We have discussed whether to do an LP every day for the past 5 days, but we do not feel the baby is clinically stable enough for that yet. Echo yesterday was unchanged from about 2 weeks ago - PFO with mild PHN. Function looks good. We are not routinely obtaining blood gases or radiographs. Prior to NIPPV, while on 5 LPM HFNC, baby had significant atelectasis, low volumes, and chronic changes. We plan for a repeat chest radiograph tomorrow to track changes, if any. Most recent CBC has trended toward neutropenia, but the ANC was still ~2500. We started more frequent and prolonged tummy-time today. I guess the kids call that "proning" these days We have considered chest physiotherapy, but worry the baby will not tolerate cup percussions. Baby remains on full feeds and oral dexamethasone, caffeine, MVI, and midazolam as needed. We lost IV access, and although it makes us nervous to not have access, we do not have a need for an IV right now. Caffeine dose is 5 mg/kg BID. At this time, we are using the DART protocol for dexamethasone. We made this decision based on our comfort level with using this regimen. However, if the FiO2 need continues to increase, we may need to rethink the dose. By limited accounts, it seems in PICUs they are using a dose about 4x the starting DART dose. It seems about once per year, we have cared for a former ELBW baby, that has never left the NICU, and acquires a viral respiratory pathogen and has clinical viremia. We are day 4 of severe symptomatology with this baby. We understand that some adult covid patients have a "honeymoon" period, lasting for 7-10 days, then can acutely become critically ill. By our experience with other VRPs, this is about the time we expect slow but continued improvement. Overall, we are trying to balance the baby's ex-premie with BPD needs with the additional support for his suspected Covid. Thus we have continued to limit blood draws, maximize nutrition, minimize radiation, continue the MVI, etc.

Three years ago, if one had asked me what I would do if I "won the lottery", I would have wanted to continue to practice Neonatology. Over the past three years, my career has been increasingly about administrative duties. I still maintain the same clinical time which is 1.5 FTEs (full time equivalents). October of this year, we added a new EMR/CPOE. And...of course, the pandemic. I am ashamed to write this, but hopefully my experience will help others. I have burn out. I wasn't even aware of it. I needed a sort of "intervention" by other physicians to point out that I was in fact suffering from, and exhibiting a lot of symptoms of burn out. These "symptoms" resulted in a very passive/aggressive behavior pattern over the past 2-3 months, culminating in me telling a set of nurses walking through the NICU without masks, "Please put on your masks. I am not f*cking around anymore." That little comment resulted in a meeting with the hospital CMO. After we discussed my behavior, the CMO basically just called me out. He said I was suffering burnout. He said I am one of many good physicians locally whose professional behavior has deteriorated during the last few months. He was good enough to point out that my bad behavior was at least motivated by concern for patient and staff safety, but that any further bad behavior, regardless of the motivation, could result in loss of hospital privileges. He pointed out that my behavior mirrored most of the physicians that he needed to counsel, and that thankfully I had not deteriorated into other more harmful symptoms like substance abuse, etc. Just some bad words said in anger. Regardless, it made the staff feel uncomfortable, and I need to be better. In discussing the issues with the CMO, then spending the evening (and this morning) researching physician burnout, I must admit, I am a little disheartened. The research suggests burnout is only getting worse, and unfortunately, the best research on the subject suggests that the biggest contributor to burnout, is also the thing that is least in a physician's control - essentially working within complicated systems that do not always make sense scientifically or clinically. A second large contributor was EMR/CPOE. Here are the personal issues I have identified: 1. I do not feel like I am being heard by administrators/managers. This has always been an issue, wherever I have been. However, during the pandemic, it has felt more acute and more urgent. 2. I do not feel supported by the community I serve. There seems to be not only a viral pandemic, but also a pandemic of scientific illiteracy in the general public and many healthcare workers. 3. I need to understand that we have all been living in a heightened state of awareness over the past few months. It is as if our sympathetic nervous systems have been in overdrive for months. I need to recognize that the sense of urgency I feel is likely exacerbated by this chronic fight/flight reaction and may in fact, be unwarranted. 4. My support system is not what it used to be. Prior to the pandemic, three close friends and their families moved away. These were friends and colleagues with whom I could vent my frustrations without causing offense. During the pandemic, it has been very difficult to replace these confidants because social interaction has been very limited, even when we are in the same area. 5. I actually have adapted to EMR and CPOE better than most. Likely this is because I have been through at least three "go live" episodes at big hospitals, thus I have come to accept that I need to just embrace the suck and do the best with the tools I have. 6. It is not the things I say, but the way I say it. This is not just in the face-to-face conversations, but also in how I interact with others within the system. I need to remember that although I may supervise NNPs, RNs, RTs, etc., I am not their employer. When I note they are doing something wrong, many times, it is best just to bring it to the attention of their manager, rather than point it out to them face-to-face. Like it or not, I am working within a complicated system, and if their is no immediate danger in someone's actions, it is best just to use the chain of command. Also, I need to remember #3 above. 7. I need to stop watching the news. Prior to the pandemic, I might skim through a daily news feed. Once the pandemic hit, it seemed news sources were just as aware of new developments as the scientific community. I found it useful to hear about a new study on the news, then search for and read the actual article(s) to increase my knowledge. The problem is, I got sucked into all the other nonsense. I do not think I am unique in this behavior, but I do need to recognize that I need as little exposure to "news" as possible right now; it fuels my frustration and heightens the fight/flight response. It is difficult to watch the daily death count, then walk into a complicated medical system, and accept hospital policies that are as much about consumer satisfaction and legal maneuvering as they are about patient, staff, and/or public safety. 8. I need to accept that many healthcare workers are not going to act in the interest of public health in their personal lives (see #2 above). I am one that believes the stages of grieving apply to many things other than death. As I have pondered it over the past couple days, I can see clearly how I went through stages of denial, anger, bargaining, and even sought treatment for depression this summer. I have struggled with situational depression, off and on, through my life. Meds don't help me. The best thing for me is realizing depression is anger unrealized. I am grieving the loss of ideals that turned out to be false beliefs. I am stuck in the anger stage. Most of my anger is focused on the poorly managed pandemic in my homeland and within the walls where I work. I do not believe that I am alone amongst scientists and healthcare providers in feeling this anger. The problem is my reaction to that anger over the past couple of months. Another issue is that I do not want to sink into a depression about the injustices I see, but cannot change. One way that has helped me in the past is just to talk about it - not complain and accuse, but rather a real gut-wrenching discussion about how these injustices (real or perceived) affect me internally. Anyway, if this topic is not germane to this forum, and needs to get deleted, I understand.

We also use: (weight in kg x 3) + 9 + length of cord This gives us an approximation of UAC depth. Half of UAC length approximates UVC depth. We use an AP radiograph to confirm placement. There is a method by which one can use the cardiorespiratory monitor to determine position of the UVC. Essentially you set the monitor to give an auditory beep with each heart beat. Advance the UVC until the frequency of beeps decreases (this implies the tip of the UVC is at the SA node), then pull the UVC back about 1/2 cm and it should be in a pretty good position. However, those I have seen use this technique still confirm with chest radiography. I would like to gain experience in POCUS as it might limit exposure to radiation.

Most I have worked with, including myself, will begin TPN as soon as possible in VLBW and ELBW babies, even with babies that have evidence of metabolic acidosis. In the larger babies, we are more likely to start a "clear" solution of trophamine, dextrose and calcium, or even just a straight dextrose solution - initially. To control blood glucose levels, mostly we can get by with just adjusting the IV rate until we can order a new bag of TPN (once daily). If adjusting the rate is not working (or we have reached a rate we are not comfortable with), we will "Y-in" an appropriate dextrose solution. Once we get glucoses under control, we will note the GIR at which that occurred, and tailor our TPN accordingly the next day. Long ago, I worked with some that would add an insulin drip to control high glucoses. I rarely see this being done anymore. My personal experience with insulin drips, especially in ELBW and VLBW babies, is that it is very difficult to predict how a baby will react. Insulin drips make for a long night of glucose checks, frequent adjustments to the GIR, adjustments to the insulin drip, and boluses of glucose. I suspect this unpredictability is exacerbated by insulin's adsorption to IV tubing. On insulin drips, I have seen glucoses vary between <20 and >200 without making a single change in GIR or insulin drip. I have yet to order an insulin drip, but have needed to manage them when ordered by others, thus my comfort level with insulin drips is minimal. In extreme hyperglycemia when we are already using D5W (in TPN) but still need volume, I have added insulin directly to the TPN. This seems to have a more predictable response. We are cautious with enteral feeds when we suspect an anoxic/hypoxic event, or in any baby with significant, or worsening, metabolic acidosis. In these babies, we generally assure renal and hepatic function are normal or substantially improving prior to initiating enteral feeds. Ultimately, it seems that the sooner we can begin enteral feeds, even if only small/trophic volume like 15-20 mL/kg/day, the sooner the blood glucoses become stable. Someone smarter than me can probably explain why, but I suspect intracellular signaling induced by enteral feeds, somehow stabilizes insulin production in the baby. Hope this helps,

Former 27 weeker, 895 gram male (now 1700+ and 36 and 6/7). STAT C-section for abruption, Apgars 1/3/5. Suspected antepartum anoxia/hypoxemia based on blood gases. Developed renal failure, elevated transaminases, etc. Very difficult respiratory mgmt, at 2 months of life, still on 5LPM HFNC and 50% FiO2 which is far outside the norm for us. This weekend, increased frequency and severity of apnea prompted a septic workup, including viral respiratory panel by RT-PCR. Negative for all the common resp viruses (including RSV, metapneumo, and flu), negative blood culture (now day 3), but positive for SARS-CoV-2. Tested mother, negative at admission, positive now. We are conducting surveillance on all staff, but right now it looks like he got it from mom. Mom now admits to some nausea and pharyngitis last week when the baby started becoming acutely ill. Mother is a healthcare worker and has not been vaccinated. Baby has moved from HFNC to NIPPV +6 and a backup rate of 35. He is dependent on the backup rate. His fiO2 need has decreased to about 30%. We started dexamethasone 2 days ago. He also had/has mild PHN as evidenced on echo last week and clinical lability. His only meds include caffeine, midazolam prn, dexamethasone, and multivitamin with Fe. We kept him NPO for about 24 hrs when he was most acutely ill, but as of this morning, he is back on full feeds. He received 48 hrs of nafcillin and gent this weekend. By my research, this is the first case of a former ELBW baby acquiring and becoming symptomatic with SARS-CoV-2 in the NICU. Has anyone experienced, or know of similar cases? If so, any special considerations for management? Is there the possibility of delayed severe symptomatology as is reported in the adult population?

Sad day. In spite of our best efforts, we have been unable to get this baby to ventilate and oxygenate. This morning, on a MAP of 10.5, this was the CXR: Last night we tried a mixture of milrinone and dobutamine to increase cardiac output and open the pulmonary vascular bed, but this made our oxygenation and ventilation worse. We stopped those meds and the baby did fairly well overnight with respect to his blood gases, and we were able to wean the amplitude somewhat. The echo yesterday showed a small PFO shunting left to right, but otherwise, no significant pathology. Throughout the morning and the afternoon, his oxygen saturation and ventilation worsened, necessitating we increase his amplitude to levels higher than last night. This was a CXR from the early evening: As compared to yesterday, the PIE has gone from micro to macro, and the hyperexpansion remains in spite of modest MAPs. This CXR was on a MAP of 11, amplitude of 32 and a Hz of 6. Baby was on 100% FiO2 and saturations were in the 60s. During the course of this disease process, I have been retrospectively reviewing the train of events. The mother was admitted with bulging bags at 23 weeks gestation, and in labor. Her labor was stopped with MgSO4 and indocin. She received a full course of betamethasone and was started on antibiotics soon after admission. Baby delivered vaginally a week later, within intact membranes and was intubated in the delivery room. All resuscitation was performed, surfactant administered, lines in place, antibiotics started, and the top of the isolette was down within 60 minutes. Looking at the PiPs, they dropped to low 20s after surfactant, but then began rising again at about 16 hrs of life. The FiO2 was between 21-25% during this time and the MAPs on volume-targeted ventilation (5 mL/kg) remained at around 7 mmHg. PEEP was at 5 mmHg. At 16 hrs of life, the PiPs climbed to the high 20s/low 30s. Because the supplemental FiO2 need was minimal, a second dose of surfactant was not given. Retrospectively, I can see evidence of PIE as early as the second day of life. My question today was: should we be basing our administration of surfactant less on FiO2 and MAPs and more on PiPs? Any thoughts?

Here is the CXR when the baby's MAP was 12: Here is the CXR when the MAP was 8: Clearly the hyperexpansion and air trapping are much worse on the second CXR with a lower MAP. Per @Miguel Pantoja we increased the MAP from 8 to 10 and have now weaned to 80% with SpO2 in the low 90s. We will continue to wean FiO2 until we reach a nadir, then slowly increase the MAP to a maximum of 12, while trying to wean the amplitude, then we will try and be patient and let the lungs heal if oxygenating and ventilating reasonably well. Ideally, I would like to get the amplitude to no more than 2x the MAP. I have a CXR ordered for the early morning and will try and post it hear to show the difference. Truly thankful for everyone who has contributed to this thread.

We started steroids 5 days ago, albeit the low-dose DART protocol of dexamethasone. I am about to start Milrinone and dobutamine to improve cardiac function. Thanks for your input.

We got the Hz down to 6, but our first attempt to wean the amplitude resulted in a pretty significant respiratory acidosis. What is really strange is that in spite of weaning the MAP from its original 14 to now 8, the hyperexapnsion by CXR is getting worse. I speculate that the air leak is not healing at all, and we essentially have thousands of little tension pneumothoraces surrounding what little areas of gas exchange the baby has; I wouldn't really call them alveoli at 24 weeks. Awaiting an echo now to assess shunting and see if an argument can be made to increase contractility with milrinone.

You may already be doing all of the following, but these are some of the things we do to prevent CLABSI: 1. TPN changes are performed as a sterile procedure; nobody is allowed within 10 feet of the bedspace without hat and mask. The RN doing the change is gowned up, hat, mask and sterile gloves. Of course, new tubing with every change of TPN 2. Standardized feeding guidelines to prevent days with a CVL in place 3. Minimizing breaks into the line for medications. Medications such as caffeine are changed to po as soon as baby demonstrates ability to tolerate po feeds (at about 60 mL/kg/day) 4. Changing from a UVC to what we call a "midline" if we anticipate the need for access beyond 5 days. A midline uses the same equipment/procedure as a PICC, but is not inserted all the way into a central vein. We treat theses as PIVs with respect to osmolarity/osmolality of TPN. Our last CLABSI was a baby who had a mild bloodstream infection which we identified as the same clone of bacteria we found in mother's EBM, but since the baby had a CVL in place, it was classified as a CLABSI - this was last year. We are not a huge NICU, but in general, about 30% of our census has had a CVL in place at some time. Based on our VON reporting, we regularly go more than one year without a reported CLABSI.

Thank you everyone for your input. In spite of continuing to lower the MAP, the CXR remains hyperexpanded. Base deficit slowly worsened throughout the day, although BP remained acceptable. The Hct is stable at 45%. I gave 20/kg of isotonic bicarbonate last night for a base deficit of -10, and the pH and base deficit improved. Awaiting another CXR this morning, if it still looks hyperexpanded, I will focus more on decreasing Hz. There seems to be some disagreement in what limited literature I can find (mostly opinions) as to whether a Hz of 12-15 or Hz of 6-9 is more beneficial. Anecdotal only, but this baby seems to be responding better to the low Hz strategy. I will get a bit more aggressive about lowering Hz today, then maybe I can start weaning the amplitude as I speculate it may be the culprit of hyperexpansion. I have used the HFJV in the past to manage PIE, with good results, certainly a much more rapid response than the current case I am managing. However, at my current facility, we do not have a HFJV. Also, we are using the SensorMedics HFOV, which to my knowledge, does not have the ability to do HFOV+VG. As to repositioning the baby, we tried this earlier this week with abysmal results. Repositioning on the SensorMedics HFOV is very difficult. I will give an update in an hour or two.

Over the past 3 hours, I have slowly weaned the MAP from 11 to 9. FiO2 has remained 80-90% while SpO2 has been 88 - 91%. Blood gas prior to weaning was 7.31/42/41/21/-5 and the CXR still looked hyperexpanded at a MAP of 11. Most recent gas on MAP 9, Amplitude of 38 and Hz of 9.5 was 7.13/69.6/45/23/-6, 90% FiO2 and 90% SpO2. I dropped the Hz by 0.5 but left all other parameters as they were. Although the base deficit is slowly worsening, he has brisk capillary refill, is urinating briskly, and is maintaining MBPs >32 mmHg without vasopressors or inotropes, thus his delivery of oxygen has not been severely compromised by accepting lower SpO2.

I took over the care of a 24 weeker who developed PIE at about 5 days of life. Baby was doing well on conventional vent (volume-targeted ventilation), when at day 3 their oxygenation and ventilation began worsening. By day 5, PiPs were in the high 20s/low 30s. By day 6, the decision was made to change to HFOV. Our attempts to wean MAP while keeping SpO2 >88% were unsuccessful. We were able to get the MAP from 18 down to 14, but attempts to wean lower resulted in worsening oxygenation. At DOL 7, I made the decision that unless we could get the PIE to resolve, we were likely going to lose the baby, so I changed the strategy. Weaning the MAP became the primary concern at the expense of FiO2 and SpO2. I am accepting SpO2 in the 80s and 100% FiO2. I am allowing hypercarbia as long as the pH is >= 7.25 and pCO2 is < 70. This has required a higher amplitude and lower Hz than I would like, but it seems to be working. Do any of you have specific experience in treating PIE with HFOV? If so, what worked and what didn't work? How did you manage the Hz/frequency? I will give an update later today.

Yes, you are correct

We use a calculation of Total Fluid per day (on day zero) based on birthweight. <750 gram = 120 mL/kg/day 750 - 1000 grams = 100 mL/kg/day 1000 - 2000 grams = 80 mL/kg/day >2000 grams = 60 mL/kg/day For us, total fluids DOES NOT include medications, flushes and boluses/transfusions, rather we have guidelines in place to minimize extra fluid in medications and flushes, and we are very judicious with respect to boluses/transfusions. We increase total fluid by 20 mL/kg/day, assuming no edema. Whenever possible, we convert IV medications to po to avoid excess flushes (and also decrease risk of CLABSI). For example, we convert caffeine to po once the baby reaches 60 mL/kg/day of enteral feeds. Our Total Fluid goal on preterm babies is 160 mL/kg/day. On term babies it is 150 mL/kg/day. We consider insensible losses to be 60 mL/kg/day for patients with oliguric renal disease. Rarely do we exceed 160 mL/kg/day of total fluid on any baby unless there are weight gain issues, with fortified feeds, in the absence of respiratory/cardiac compromise. As I have gained experience, I rarely follow daily electrolytes, unless there is evidence of excessive weight loss, weight gain, poor urine output, or IV fluids lacking electrolytes. Essentially, I consider the kidneys to be smarter than me. Too often I see Neos getting daily electrolytes; on Monday they increase the Na, Tuesday they decrease the Na, increase the K, fudge the Ca, Wednesday they increase the Na, decrease the K, fudge the Ca, etc, etc, etc. At the end of the week, the baby has had 10% of their blood volume removed because of "tinkeritis". Labs beget labs, then they beget blood transfusions. We consider birthweight the calculable weight until the baby exceeds the birthweight, without signs of edema. Fluid restriction has no evidence to promote the closure of a PDA, and as long as total fluid is < 180 mL/kg/day, I have found no evidence that excess fluid volumes increase the length of time to close the PDA and affect respiratory status. In my readings/experience, PDA closure is more about minimizing inflammation, rather than fluid balance. We are strong advocates of enteral feeds and human-milk products vs. bovine-milk products. All the best!

Was there a transient improvement in SaO2 and FiO2 after surfactant administration, say for 2-4 hours? If so, I would consider a surfactant protein mutation such as heterogenous SPB mutation or homogenous/heterogenous ABCA3 mutation. Also SPC mutations are highly variable in their presentation(s). Homogenous SPB mutations may have a brief response to surfactant, but will inevitably return to a severe RDS clinical picture. Heterogeneous SPB mutations may be survivable if the baby is full term. Heterogeneous ABCA3 mutations are survivable if not premature while homogenous ABCA3 mutations are often fatal, even in full-term babies. Recommend searching papers by N. Nogee and A. Hamvas Another thought, the penetration of the Xrays may not have been optimized for the type of CXR; thus the CXR looks abnormal while the CT is normal. Does the "whiteness" of the stomach bubble correspond to the "whiteness" of the lung? if so, the CXR was probably under penetrated. if the stomach bubble is much blacker than the lung fields, there is a problem with the lungs.

I queried one of my RTs this week, asking, "why are they not using HFOV as a lung protective strategy?" Essentially the answer was that HFOV is considered a rescue ventilator mode, and once they are on HFOV, they are calling for ECMO. The adult ICUs are using Vt of ~5mL/kg, but the PEEPs and PiPs to achieve that Vt is astonishing. Done properly, HFOV need not be a rescue therapy. With the increased focus on really good neonatal ventilators, especially those that can reliably provide volume-targeted support for babies < 1000g, I find myself using HFOV less and less. However, if my options were a PEEP of 20 (realistically 7 in neonate) or HFOV, I would opt for the HFOV every time.

To answer my own question (5) https://www.frontiersin.org/articles/10.3389/fped.2020.00206/full#B16 It is mostly speculation by the authors, but very interesting nonetheless

During Covid-19, I have spent more time researching Adult pulmonary critical care than Neonatal pulmonary critical care. Based on this blog: https://emcrit.org/category/pulmcrit/ I am both fascinated and disgusted by the approach to respiratory support for Covid-19 patients. For those that have been following adult pulmonary critical care: 1. Are you appalled by the PEEP and PiPs? 2. Are you appalled by the FiO2s? 3. Do you feel like this is Neonatology circa 1990? 4. Do you think HFOV and/or NBCPAP are tools that should be applied earlier, not later for Covid-19 patients? 5. Do you have a hypothesis as to why neonates, who are inherently immunocompromised, are not more severely affected? Thank you

Unfortunately, the very few N95 masks we have available are limited to the adult side of the hospital. 30 miles away, they are using N95 masks in the NICU.