By now if you have a preterm infant in particular who has been born before 36 weeks you will have heard people talking about chronic lung disease (CLD). Sometimes they may also refer to it as bronchopulmonary dysplasia (BPD). The terms are really for all intents and purposes the same from a parent’s point of view. If you google CLD or BPD you may find stories of very cystic and damaged lungs with babies needing tracheostomies due to long term need for ventilation. While this can still happen, thankfully this new type of CLD we see is not like the one of old but rather is a newer entity that is more uniform and has less of a cystic nature. The “New BPD” is really more of a lung that has less air sacs (alveoli) than usual but the lung is less damaged than the BPD of old.
When your infant was born they may have had immature lungs without enough surfactant. Surfactant is kind of like the engine oil of a car. It helps to make the lungs less sticky and allows breathing to be a lot easier. Some babies are treated with CPAP while others need intubation and ventilation. While this positive pressure can be lifesaving, it also exacts a cost. We humans prefer to breathe using negative pressure meaning that we suck air into the lungs rather than have it pushed in. With each delivered breath the lungs of these fragile infants can be injured leading to the type of picture shown above.
This becomes a concern at 36 weeks. You may hear doctors talking about 36 weeks as if it is scary deadline that is on the horizon. We tend to obsess about that date. The big reason for this obsession is that units compare themselves across Canada and in other countries using the need for oxygen, nasal prongs, CPAP or ventilation at this time point. If your unit has a rate of CLD of 10% and another has 20% it tells the higher one that they better do something with their medical practice to lessen the incidence. In other words the 36 weeks is a marker.
As I have written about in another blog post, in 2020, 40 weeks may be the more relevant number as written in the post “The New BPD That Matters” the reality is that your baby is more likely to stay in hospital due to inability to feed orally or from apnea of prematurity. I am not saying that we as a team should not try and reduce the risk as much as possible for CLD but in case you were wondering what we are talking about when we talk about this condition this is it.
Our ability to breathe regularly is something most of us take for granted. We owe this function to a tiny area in the brain located in the medulla oblongata.
This area of the brain sends signals via nerves to the lung telling it to breathe in and out on a regular basis. For a preterm infant or even term baby this means there should be about 40-60 breaths per minute. Preterm infants are at risk for these events due to being neurologically premature but also due to a difference in the responsiveness of such infants to carbon dioxide levels in the bloodstream. In term infants and throughout life we are very responsive to higher levels of carbon dioxide. We like to keep it pretty tightly controlled which is why if you hold your breath and your carbon dioxide levels rise you feel like you need to take a breath. In preterm infants this response is blunted.
Pauses in breathing are called apnea and when they occur in a preterm infant they are known as apnea of prematurity. These are usually defined as stoppage of breathing for 20 seconds or longer or if shorter there is bradycardia (<100 heart beats per minute), cyanosis (bluish color to the skin), or pallor. They are so common under 37 weeks that I consider them a normal part of the preterm journey. You can see how common it is in the figure below. We also know that they are far more common as gestational age decreases so that a 24 week gestation preterm infant will be far more prone to apnea than the 35 week counterpart.
often wonder if these drops in oxygen or heart rate are harmful. If the
events are called spontaneous it means that your infant recovers quickly from
these events without anyone stimulating your baby and so they are brief.
We tend not to worry about these types of events as they brain is not
likely to be affected. When events are happening more than a few times a
day and require your nurse to either stimulate your infant or require support
with a bag and mask to help your baby breathe this is where we become more concerned.
Even then the presence of bradycardia during these events is more
concerning than the oxygen levels as the poor heart rate means less blood is
going to the brain. It is hard though to determine exactly how many
events a day are actually harmful but intuitively if they are happening more
than a few times a day and needing support to recover this is where we usually
think about treatment.
The treatment of choice is caffeine. The same drug that is present in your soft drinks or coffee. It works by stimulating that centre in the brain that I talked about above. There are different dosing levels but you will see doses anywhere form 2.5 mg/g/d to sometimes 8 mg/kg/d for those babies with very resistant apnea. Some of those kids may need CPAP (mask on the nose) or intubation and a ventilator if they just won’t breathe. The good news is that they will grow out.
Most of our babies have their caffeine stopped sometime after they have reached the equivalent of 33 weeks (eg. born at 26 weeks this would be 7 weeks later). On rare occasion babies right up to term will have apnea as shown in the graph and for those kids if they are feeding well and otherwise ready for discharge we may choose to send you home on caffeine. Those kids though will need a follow-up study called a sleep study that will typically be done about 4 weeks later and require your child to come back for the appointment.
Aside from me donning the costume in the above picture for the Kangaroo Challenge 2017 I learned something new today. Before I get into what I learned, let me say that I had the opportunity to put so many smiles on parents faces by walking around in this full body costume that I am grateful to Diane for finding this costume and Sue (you both know who you are) for purchasing it. Handing out cookies to the parents and children at the bedside and seeing them smile while knowing that they were under significant stress gave me the opportunity to interact with parents in a very different way than I am accustomed to as a Neonatologist so I am so thankful to have had that experience and yes if called upon I will do it again!
I posted the above picture on my Facebook page and to my surprise many of the comments led me to believe that Kangaroo Care is still something that needs a little nudging to get the word out about. I found this actually quite surprising given how immersed we are in Winnipeg with this strategy. When I think about new interventions in Neonatology it is synonymous in virtually all cases with an influx of dollars to achieve usher in the new program. Here is a program that is virtually free but only requires a commitment from families to spend the time at the bedside with their baby in the NICU.
I have been asked by many of my nursing colleagues to write something about Kangaroo care on this site and so here it is…
What is it?
You have likely heard of Kangaroo Care and you may have even seen some children receiving it in your hospital. Why is this so important?
Kangaroo Care (KC) or Skin to Skin Care (STS) is an ideal method of involving parents in the care of their premature infant. It fosters bonding between parents and their hospitalized infant, encourages the family to be with their child and thereby exposes them to other elements of neonatal care that they can take part in. While we know that many units are practising Kangaroo Care there is a big difference between having KC in your unit and doing everything you can to maximize the opportunity that your families have to participate.
There is much more to KC than simply holding a baby against your chest. For a demonstration of KC please watch the accompanying video and show it to any one in your units that may need a visual demonstration. This excellent video is from Nationwide Children’s Hospital and walks you through all of the important steps to get it right and maximize benefit.
Before you reach the conclusion that KC only serves to enhance the parental experience it does so much more than that. The practice began in Bogota Columbia in 1979 in order to deal with a shortage of incubators and associated rampant hospital infections. The results of their intervention were dramatic and lead to the spread of this strategy worldwide. The person credited with helping to spread the word and establish KC as a standard of care in many NICUs is Nils Bergman and his story and commentary can be found here http://bit.ly/1cqIXlm
The effects of KC are dramatic and effective to reduce many important morbidities and conclusively has led to a reduction in death arguably the most important outcome. An analysis of effect has been the subject of several Cochrane Collaboration reviews with the most recent one being found here.
To summarize though, the use of KC or STS care has resulted in the following overall benefits to premature infants at discharge or 40 – 41 weeks’ postmenstrual age:
mortality (typical RR 0.68, 95% CI 0.48 to 0.96)
nosocomial infection/sepsis (typical RR 0.57, 95% CI 0.40 to 0.80)
hypothermia (typical RR 0.23, 95% CI 0.10 to 0.55)
KMC was found to increase some measures of infant growth, breastfeeding, and mother-infant attachment
To put this in perspective, medicine is littered with great medications that never achieved such impact as simply putting your child against your chest. This is another shining example of doing more with less. This is not to say that modern medicine and technology does not have its place in the NICU but KC is simply too powerful a strategy not to use and promote routinely in the NICU.
Please join me in championing this wonderful technique and make a difference to all of our babies!
A sample of our parent letter to promote KC is found in the link below.
Those are the first words that a parent given the diagnosis of stroke says after hearing the news. It is perhaps one of the worst nightmares a new parent can have. A baby is carried to full term and is born after a seemingly uneventful delivery with normal apgar scores. The family spends the first day together getting to know each other and planning for life outside the hospital. Then sometime between the first and third day of life the parents note their infant shaking an arm or leg repeatedly and call the nurse for assistance. A physician arrives and informs the parents that she believes their newborn is having a seizure and orders phenobarbital, which the parents have never heard of. Shortly afterwards, the family is told that their child needs an MRI and an hour later when the report comes in their world is shattered as they are informed that their infant has a stroke.
At this point their minds flood with memories of elderly relatives or assisted living homes where they met people with strokes and with that their world and dreams are vanishing in front of their wyes.. Lost is the sense that they will have a normal child when they go home but is this what they should expect or is the experience of the family in the following video what is more likely to occur. Such a story told through the experience of a family in this TED talk so well captures the essence of these feelings that I urge you to watch it before moving on.
Shocking as it may be to hear that a newborn has had a seizure, the reality is that the frequency of such events is no different than in adults. Moreover the newborn period has the highest rate of stroke than any other time in childhood. The overall incidence of neonatal seizures is between 1:2000-3000 live births.
Stroke in a newborn is frightening and from the International Pediatric Stroke Study we have the following figure that provides information as to what these children present with. The symptoms usually present as they did in the case above sometime after 24 hours and consist of the following.
How do they do in the long run?
We are fortunate that the group from Hammersmith has been following a group of neonates since their diagnosis of a middle cerebral artery infarction more than 15 years ago and intermittently reported on their neurological outcomes. In the most recent report at age 9 years published in 2008 the results indicated that of the original cohort of 31 patients about 30% had hemiplegia. Interestingly with respect to cognitive outcome the results were just as promising or perhaps even better in that 21/27 assessed at 9 years had normal intelligence. Of the six children who had an IQ below normal, the lower results may have been explained by something other than a neonatal stroke. Two patients were dysmorphic but without a specific diagnosis, one child had autism, one was too shy to be tested so perhaps had normal intelligence and the last child had signs on the original MRI of significant ischemic damage to the brain stem suggesting an additional insult over and above the arterial stroke.
In the Hammersmith cohort almost all patients suffered a left MCA infarct which for reasons that remain unknown is the most common territory affected. The next most common location is the posterior circulation and was the subject of a paper by L de Vries on outcome at a mean age of 36 months.
Out of the 17 patients followed, 5 had a global delay with 9 having visual defects. The presence of visual defects is not surprising given the finding that the infarct in the posterior circulation caused injury to the periventricular white matter. This area of the brain of course is where the optic radiations pass through leading to such a disability. Interestingly only one of the 17 that were followed had a hemiplegia.
As you can see the likelihood in the newborn with a stroke is that they will recover their motor function a great deal and unlike the adult with a similar stroke they are capable of a “rewiring” that provides hope for those parents after the initial devastation of hearing the word “stroke” for the first time.
What features provide a high likelihood of later impairment?
As was shown by Mercuri et al in 1999 the existence of a stroke involving the basal ganglia, internal capsule and hemisphere is predictive of motor impairment. The basal ganglia and other structures mentioned are comprised of several different areas that are labelled in the picture of the brain and are comprised of the putamen, caudate, globus pallidus, the substantia nigra, nucleus accumbens and subthalamic nucleus (the last three not labelled below). Injury to any of these structures along with the internal capsule and other area of the hemisphere would not have a probable good outcome.
Additional work done by the International Pediatric Stroke Study in 2011 indicated that the following features were predictive of adverse outcome.
It is important to note that this was outcome at discharge for 250 neonates with stroke. It will be interesting to see if the 50% motor impairment at discharge in this cohort diminishes over time as in the Hammersmith group.
So when we look back at the video that is featured in this post I question whether this family was given good information at the outset. Maybe if someone had put together a post like this to share with them (and to put it into slightly more lay terminology) they would have had fear replaced by cautious optimism.
Who knows maybe this post will reach someone and spare them some of the anguish that I imagine this family must have faced?