It’s Father’s Day so why not put out a post about a role for father’s in resuscitation. Given that we are talking about a parent being present for resuscitation after delivery and the mother will have just delivered, what follows is a discussion about having the other parent present at the ensuing resuscitation if needed. This will of course not always be a father as in female same sex parenting so what follows could apply to any situation in which there are two parents present and one has just delivered.
Since I was a resident this question has been batted around. During a resuscitation is it better to have families present or not? Certainly work has been done in this area which has demonstrated that from the families perspective this is a worthwhile pursuit. Families wish to be present and as a parent myself I would say it would be far more frightening to be kept out of the room than invited in to see what is going on. A mind can often conjure up scenarios that are far worse than actually exist if left to ourselves. I think in many centres now this is the case that families are invited into the room when their infant is being resuscitated but looking at things from another standpoint the question becomes what effect this has on the team doing the work? Does the team perceive that their workload is increased and if so could this affect performance?
An Answer to this question?
Dr. Schmölzer and his team in Edmonton (my former place of work) have atttempted to answer this question by looking at initial resuscitations in the delivery suite. Their study Does parental presence affect workload during neonatal resuscitation? used a tool I was unfamiliar with called the multidimensional National Aeronautics and Space Administration Task Load Index (TLX) survey to assess workload. After a resuscitation team members were invited to fill out the survey anonymously and in total 204 submissions were done. Degree of intervention after delivery included requiring stimulation 149 (73%) and suction 130 (64%), 120 (59%) continuous positive airway pressure, 105 (52%) positive pressure ventilation, 33 (16%) intubation, 10 (5%) chest compression, and 4 (2%) reported administration of epinephrine during resuscitation.
Results and Thoughts
Looking at the raw scores on the TLX the difference was highly significant in favour of having a parent present.
When further subdividing by apgar scores an interesting finding emerges in that as the apgar score increases the workload decreases. Even in the lowest apgar range the workload though appears to be equivalent.
I wonder if the finding results from being able to kill two birds with one stone? Part of the duty for any health care provider performing a resuscitation is to inform the parent of what is happening. When a patient is not doing well a provider might feel distracted and torn between providing the immediate care required and keeping the family abreast of what is happening. Having the family member present to see exactly what is going on reduces the amount of communication using descriptions and having to explain what they mean. Being able to point at an infant on CPAP and having respiratory distress for example is far easier with the parent present to point at the finding of indrawing than taking the time to explain it. I suppose the number of questions might even be lower in that circumstance. If a baby is quite ill at birth though and receiving chest compressions or epinephrine I would imagine it would be difficult to educate the family concurrently so explaining in detail what has been happening might be deferred to a later time point and hence the workload might be no different. What the data does suggest to me though is that in addition to previous research demonstrating benefits of families being part of the resuscitation for themselves, the team is no worse off in terms of workload and might even benefit from having them there as well.
The next logical study will look at resuscitations on the unit rather than in the case room but I think the question that was talked about as a resident can be put to rest.
Phototherapy is one of the “bread and butter” treatments in the newborn. For sure it has gone through changes over the years as different light sources have been developed that provide more limited spectrums of blue/green light wavelengths. Gone are the old long white tubes in favour of special blue light emitting banks of lights and with it bilirubin levels are effectively dropping quickly worldwide. There have been a couple concerns raised with phototherapy over the years. One concern has been the risk of DNA damage as shown by Ramy N et al in Jaundice, phototherapy and DNA damage in full-term neonates. It was found in this study that the duration of phototherapy but not it’s intensity were related to the extent of methylation of DNA which is a marker of damage. Shorter durations would therefore be preferable. Repair of damaged DNA is thought in some ways to contribute to risk of cancer so although this has not been demonstrated with phototherapy the concern has been raised before. The other concern pertains to the ELBW infant with very thin skin. In the randomized trial for babies under 1000g entitled Aggressive vs. conservative phototherapy for infants with extremely low birth weight. In this trial a lower threshold for starting phototherapy was used in the “aggressive group”. The findings of this study in a preplanned subgroup analysis was that the babies from 500-750g that had a lower threshold for starting and continuing phototherapy had a trend towards a higher mortality; relative risk, 1.13; 95% CI, 0.96 to 1.34 as the CI just crossed 1. With this information in the literature it stands to reason that the question would come up as to whether continuous phototherapy is needed or whether one could use cycled intermittent phototherapy to give infants “phototherapy breaks”.
Such a study has now been published
This study enrolled babies with birthweights between 401 – 1000g and Initially randomized using a 1:1:1 ratio to 3 treatment groups: continuous PT (usual care), a PT regimen of 30 minutes or more per hour for each cycle, or a PT regimen of 15 min/h or more. The minutes per hour of PT could be increased for the cycled if TSB values reached specified thresholds. After the first 100 patients a planned analysis was done and the 30 minute group was ended as there was no difference between this group and the 15 minute one. The light sources and spectral irradiance (combination of intensity and distance from the patient) used were all the same and collection times for serum bilirubin levels were standardized as much as possible. Bilirubin levels were collected daily for the first 7 days and anytime infants were on phototherapy. The authors also included a stepwise prolongation of phototherapy for the shorter cycled groups if bilirubin levels were not responding to the provided phototherapy. I have to say they really did a good job of removing as many potential variables to outcome as they could!
The primary outcomes were mean peak TSB levels and mean PT hours through day 14 across all centers and predischarge wave V latency brainstem auditory evoked potential (BAER). In total 305 infants were randomized in the study and the interestingly the study was stopped at that point as a larger study was approved to obtain more precise estimates in the future around mortality and morbidity as a primary outcome. During the trial the authors received approval to do so with this new primary outcome and so we have what we have to analyze.
The authors found that there was no difference in the mean peak bilirubin even among high risk patients when given cycled phototherapy for 15 minutes an hour vs continuous. The total amount of hours of phototherapy was approximately halved. No statistical difference in mortality was observed although as mentioned above this was not the primary endpoint of the study.
Looking at duration of phototherapy in terms of hours per day over the first two weeks is shown below. Although a pre-specified plan was in place to increase time as needed to decrease bilirubin levels the amount of time remained fairly consistent for the cycled group with some increase needed in the early days which would be expected given the typical higher biirbubin tendency in the first week of life.
The BAER tests did not demonsrate any difference between the children who had cycled or continuous phototherapy suggesting that no added neurotoxicity occurred from interrupting phototherapy.
What can we take from this?
All of these infants were ELBW and wth that had very thin skin. Would cycled phototherapy be as effective in more mature infants? As the authors of the study point out, there have already been several trials in more mature infants demonstrating such effects and arguing that continuous phototherapy is not needed. At the very least this paper and the others before it would argue that interrupting phototherapy to allow breastfeeding or some skin to skin time with the mother or father should be acceptable. In the past I can remember many instances of having ordered intensive phototherapy and then questioned whether mom can breastfeed as technically it is supposed to be continuous. With this information I would suggest that continuing to work on oral feeding skills at the breast is reasonable. Clearly this won’t work in the population studied here as they are too small but for the larger infants there would not seem to be harm.
I suspect the larger study to come may change practice if a higher mortality is indeed shown for continuous phototherapy but for now we will need to wait and see. In a few years we will get the chance to review that study here.
It isn’t often I have had the pleasure of reviewing a paper from my own center (maybe because I have been reticient to critique my colleagues) but this paper I couldn’t resist. If my colleagues are reading this then I will provide a spoiler alert that I am not planning on trashing the paper. A few years ago my colleague Dr. Yasser El Sayed (who many of you will know from his work on targeted echocardiography and ultrasound and most recently on www.pocusneo.ca) began touting the benefits of vasopressin as an inotrope. I have to confess, my knowledge of the drug was mostly at that point as a molecule that helps regulate water balance at the level of the kidney. As the saying goes you can’t teach an old dog new tricks so I suppose it has taken me some time to get around to embracing the other benefits of vasopressin. As an inotrope it has some interesting properties. It is through action on two different receptors that the appeal of this medication is derived. Firstly it acts on V1 receptors of blood vessels, causing vasoconstriction on the systemic side and supporting blood pressure and almost paradoxically in the lung at the same receptors, causes pulmonary vasodilation mediated by the endothelial release of nitric oxide. In the kidneys, as mentioned above it helps in water reabsorption through its action on V2 receptors. In other words it supports both the systemic and pulmonary vascular systems and maintains intravascular volume by preventing hypovolemia. That is a drug with some interesting properties.
Case Series From Winnipeg
One of our previous fellows Thomas Budniok authored Effect of Vasopressin on Systemic and Pulmonary Hemodynamics in Neonates along with Dr. El Sayed and Dr. Deepak Louis. This was a retrospecitve case series from 2011-2016 looking at patients who received vasopressin and I am delighted to say I cared for many of these babies so saw firsthand how the drug worked. The drug was typically used as a second or third line agent for hypotension and would be also be used when pulmonary hypertension complicated systemic shock as well (in addition to use of iNO). To look at the effect of vasopressin on hemodynamics, the authors used a previously validated score called the vasoactive inotropic score (VIS) = dopamine dose (μg/kg/min) + dobutamine dose (μg/kg/min) + 100 X epinephrine dose (μg/kg/min) + 10 X milrinone dose (μg/kg/min) + 10,000 X VP dose (U/kg/min) + 100 X norepinephrine dose (μg/kg/min). By looking at changes over time this gives an impression of the effect of the drug on other inotropic requirements. The authors looked at 33 episodes in 26 patients with a median starting dose was 0.3 mU/kg/min (IQR: 0.2–0.5).
While the starting dose was 0.3 mU/kg/min , the maximum dose was 0.65mU/kg/min (IQR: 0.4–1.2) with a duration of therapy of 37 hours (IQR: 21–69).
As you can see from the first figure of the paper, mean, systolic and diastolic blood pressures all rose over time. Might this be though that the infants were just getting better or we were using other inotropes to get the effect? Also as the measurements were taken at baseline and then 6,12 and 24 hours the influence of other measures might be expected to be less but it is the VIS that may yield more information.
Maybe not surprisingly, given the changes in blood pressure the following benefits to lactate and pH were also noted.
The VIS scores declined from 15 (9–20) to 13 (7–20) and 10 (8–16) at 24 and 48 hours post starting of vasopressin. Although not signficant, the median number of inotropes in use went from 2 to 1 after 24 hours.
As good as the medication seems to be the authors noted hyponatremia in in 21 episodes (64%) with severe hyponatremia in 7 episodes (33%). Personally I can comment that I stopped vasopressin myself in a couple patients due to this complication.
I suppose it goes without saying that future studies will need to look at vasopressin using a control group. Having said that I do believe this study provides some decent evidence of effect. The short time frame of analysis and the significant changes in hemodynamics and markers of perfusion with a reduction in dosing of additional inotropes suggests a decent effect of this drug. If you choose to use this medication however what prevents this from being the “perfect pressor” is the limitation of possible hyponatremia with its use. Hyponatremia though may be seen with higher doses so I suppose the saying may apply that with vasopressin a little may go a long way!
Peripherally inserted central catheters (PICCs) are pretty common in NICUs these days. As time has gone by, patterns have shifted in many units from having many people placing PICCs to dedicated teams. This makes a great deal of sense as the more learners you have the less the individual experience one gets and potentially the lower the success rate. Additionally concerns may arise from complication rates which may due to less experience creep up in frequency. Another question that you might ask is whether there is a difference in rates of complications depending on whether a PICC is placed in an upper or lower extremity. As it turns out a colleague of mine in Wisconsin took a look at this from his time in Seattle and has published the following paper Risk factors for peripherally inserted central catheter complications in neonates. The findings of this large cohort of patients I think is informative and worth a comment!
What Type of Study Was This?
This was a retrospective review of neonates less than 28 days old using the electronic medical record from Seatle Children’s and University of Washington Medical Center. All PICC placements were done by a nurse driven PICC line team. Confirmation of placements was via x-ray unless it was an interventional radiologist (7.3% of placements) placed line in which case ultrasound was used to provide accurate placement. Proper positioning for upper extremity placement was considered to be for “lower extremity lines if the catheter tip was above the inferior vena cava bifurcation. Upper extremity lines were considered to be in a central position if the catheter tip was in or proximal to the brachiocephalic vein for (distal subclavian was sometimes considered central as well by medical team).” The primary outcome of interest was nonelective line removal. The reason for sharing the information here is the size of the study. The authors were able to look at 918 subjects and 1234 PICC lines and look at outcomes to answer their primary question and also indentified some interesting secondary outcomes.
What Did They Find?
First of all, lower extremity lines (57.5%) were more common than upper extemity (42.5%). The patients covered a range of weights from 0.5 to 6 kg with the most common lines placed being 1.9 or 2 Fr and the average length of line use was 10.6 days.
“Overall, 28.4% of all lines were removed nonelectively and 34.4% of lines were associated with a complication”
What sorts of complications did they find?
Secondary outcomes. Is there a difference between upper and lower extremity placement?
It turns out, lines were more likely to be removed non-electively if they were placed in upper vs lower extemities and the difference was found to have an OR of 1.73 with high significance. Malposition in the first 24 hours was also found to be higher or at any time. The risk of extravasation was also noted to be higher with a OR of 4.49 if placed in upper extremities. Phlebitis or edema was found to be higher in lower extremity placement.
When looking at risk factors for failure the following was seen.
Intra-abdominal processes such as NEC increase risk for any complication and non elective line removal as does need for surgery or provision of TPN.
What Can We Do With This Information
The information first off may not apply to all centres as the types of patients will vary from place to place. It is worth speculating on the higher failure rates in upper extremity placement though. Looking at the anatomy of the upper extremity vessels vs the lower, there may be a longer stretch of straight blood vessels in the lower extremity to work with. As an infant grows if the line pulls back a cm or two in the IVC it is still likely in the IVC. The same is not likely true of the upper extremity venous system.
The distance in a small preterm infant from a well positioned line in the inominate vein to the subclavian or axillary vein is not far. It is not hard to imagine that with growth the tip of a line can migrate back to one of these smaller blood vessels so complications such as extravasation may become more common. Curiously one thing that appears to be protective though is a line staying in beyond the mean of 10.6 days. It would be easy to suggest that that disproves the theory I have provided but perhaps the message here could be that while the lines are more prone to migration in the uppper extremity, if they don’t and last beyond the mean they are unlikely to be problematic. Lines that are destined for failure seem to do so early.
Taking it all together though it would appear that if one had a choice of either upper or lower extremity to place a line, in the absence of an intra-abdominal process it just might be better to go with lower extremity placement. I wonder how this compares with other centers out there?
If you have had a baby born prematurely and are reading this blog post you may have been told that the medical team is looking for a PDA. The PDA stands for Patent Ductus Arteriosus and the last two words Ductus Arteriosus really helped your fetus as it was growing in the womb. In order to understand how it can cause a problem after birth it is first important to understand what it did and why it exists in the first place.
Act I – The Womb
When your baby was developing its lungs the tissue was busy branching into airways that ended in little air sacs called alveoli. Each of those alveoli was next to a capillary which is our smallest blood vessels in the body. One day these units (alveolus and capillary) will happily exchange oxygen that is breathed in for carbon dioxide that needs to be breathed out. In the womb though the lungs were filled with fluid and air was nowhere to be seen. As such, most of the blood (about 90%) that came back from all the veins in the body to the right side of the heart had no business going to the lung. There was just not really any point in sending blood to the lung when it couldn’t pick up any oxygen there. The fetus by having a ductus arteriosus had a “pop off valve”. Since the pressure in the lung was high instead of sending blood to the lung, the 90% went from the right ventricle in the lower part of the heart to the pulmonary artery and from there across the ductus arteriosus to the aorta. The blood following this path therefore basically bypassed the lung and went from the “right” side of the heart to the “left” side that normally sends blood with oxygen to the rest of the body. The oxygen in this case came from the placenta. This fetal ciruculation is shown in the figure below.
Act II – Life on the outside
After birth the lungs fill with air containing oxygen and the resistance to blood flowing into the lung decreases which is a good thing as it allows oxygen to move from the alveolus to the capillary and back to the left side of the heart. As oxygen in the blood stream rises this usually leads to closure of the ductus arteriosus. In preterm babies though the ductus may not shut and this is what we call a Patent Ductus Arteriosus or PDA. This becomes a problem when the blood pressure in the aorta is high and the pressure in the lungs falls with breathing of air. Eventually, instead of the right to left flow of blood that occurred before, you now get blood flowing from the aorta to the pulmonary artery going to the lung and as more and more blood flows to the lungs they start to look white on chest x-rays and it gets harder and harder for your baby to breathe. The mixing is shown below.
Act III -So what do we do about it?
If we suspect that there is a PDA your doctor will order a test called an echocardiogram. This is an ultrasound of the heart and may be done by a specialist in the heart called a Cardiologist or may be done by a Neonatologist trained in doing such tests. Either way if the doctors believe the PDA is causing problems they will suggest a treatment plan to deal with it. The problems that would tend to motivate us to treat would most commonly be that your baby is needed support to help their breathing although problems related to poor blood supply to the kidneys might also lead us to treat.
The mainstays of treatment are two very common drugs and one that you may not have heard of. Indomethacin is a drug that was first used to help close PDAs and is a non steroidal anti-inflammatory (NSAID) drug that is in the same class as ibuprofen (advil) which is another drug that is used. In some centres another very common drug acetaminophen (tylenol) is employed. Most centres at this point are using one of the first two. Regardless after the medicines are given the doctors will order another echocardiogram to see if the PDA has closed and if not may repeat a course of the same medicine or choose a different one.
Act IV – What do you do if it just won’t close?
The next steps depend on how your baby is tolerating the PDA. If your infant is breathing on their own and their kidney function is working well many doctors will just observe and not offer more treatment. Babies though who are on a ventilator or are having significant issues related to their kidneys may rarely need to have a surgeon put a clip on the PDA to close it. These days this is quite rare and there are some centres that choose to not treat the PDA with medicine or surgical closure at all and just wait it out until they are gone. Almost 90% of them will close on their own if you leave them alone but again it depends on how sick your infant is in order to determine if this is reasonable.