Hi, my name is Diane Schultz and Michael has asked me to write a series of posts on his blog about Kangaroo Care (KC). Seeing as I am one of the Champions (they call you that, but sometimes the word begins with a B) for KC in my unit, I was thrilled. I thought I would begin with an introduction as to why I want to write about this.
I have been a Neonatal Nurse for 29 years working in the NICU at St. Boniface Hospital in Winnipeg. I felt that I had always given good care to the families but did not really make connections with them.
I was fortunate enough to meet Dr. Susie Ludington about 10 years ago at an Academy of Neonatal Nursing conference. She was a general session presenter and was speaking about Kangaroo Care. The first thing she said was “My goal is Kangaroo Care 24/7”. All I could think of was WTF!? I would have to listen to this Nutbar for an hour? Our unit had been doing KC for years but only occasionally and usually the parent would ask for it, we certainly did not promote it or do it with our more fragile infants.
After listening to Dr. Ludington present, my world changed. What she said hit a cord; she presented benefit after benefit with rationale and evidence that made complete sense to me. I felt guilty I had not been doing this at work and guilty that I had not held my own daughters this way. I am now lucky to be able to call Dr. Ludington a friend, and know she has changed my life.
Now, there is a lot of evidence out there touting the benefits of KC, but the real way to understand and believe in it is to do it. KC creates its own evidence. Every time I bring out a medically fragile infant to be held in KC, I know that this is the right place for that infant to be: with their parent being held. You can see the relaxation on all of their faces (decreasing cortisol), the infant is able to go into a deep sleep (promotes brain maturation), and the family is able to connect in the best way possible. I feel KC is as important as anything else we do at the bedside and is an extremely necessary therapy.
Promoting KC in my unit has benefited me at so many levels; I believe it has actually saved my career and given me a focus that I didn’t have before. You can’t help but make connections with your families, and these families are able to make connections with their little ones. KC is also a very important part of Family Integrated Care, as this is something that the family can contribute to their child’s care.
I also couldn’t be more proud of my unit; the staff I have the pleasure to work with are some of the best health care professionals around. They make every effort to bring our fragile infants out for KC and it has become part of our culture in our NICU. KC happens in our unit with almost all of our infants, the only exceptions being actively cooling babies and infants with chest tubes. We have also created a Standard Work Protocol so all medically fragile infants come out the safest way possible without creating extra stress on the infant or family.
In my series of posts I will present the many benefits of KC for infants and their families and share some of my experiences. I hope you will be able to take something away from this, begin to try KC in your own unit, and create your own evidence.
We hope to provide education through links to publications and videos demonstrating the benefits of adopting POCUS! Less ionizing radiation and enhanced diagnostic accuracy are just two of the benefits of using such techniques. Videos demonstrating and discussing this technique can be found on the Point of Care Neonatal Ultrasound Playlist on my Youtube channel
Use of point of care ultrasound has expanded over the last decades particularly in intensive care to the point that it is now readily available for use by the clinical care practitioners in this setting (1). Today clinicians are using ultrasound at the bedside to assist in the evaluation of physiological abnormalities in a number of body systems. Ultrasound has been used to image body organs for over 50 years (2). It is currently the most widely used imaging modality in medicine. Advantages are that ultrasound is portable, free of radiation risk and relatively inexpensive compared to other diagnostic modalities like magnetic resonance and computed tomography (3). The main limitation when considering this for use by NICU clinicians is that it requires advanced training. In addition, when compared to traditional x-ray, ultrasound has limited penetration to air and bones and therefore structures deeper to them cannot be well assessed (4).
There are three general indications for ultrasound in the neonatal setting:
1) Anatomic assessment of static organs such as the brain, lungs, liver, kidney and spleen to evaluate for anomalies, hemorrhage, space occupying lesions and abnormal fluid collections.
2) Dynamic assessment of moving organs, such as the heart, lungs, intestine, and the vascular system to evaluate blood flow and physiologic processes.
3) Locating vessels for cannulation and determining the position of catheter tips.
Anatomic ultrasound assessment of static organs should be provided by a trained radiologist. Dynamic ultrasound assessment can be performed by a trained neonatal clinician who understands the clinical details of his or her patients and is familiar with the underlying pathophysiologic mechanisms (5). Table 1 shows different applications performed by a trained clinician.
Point of care lung ultrasound:
In the last 10 years, research studies have shown that lung ultrasound (LUS) is an accurate, non-invasive method for predicting ventilatory failure and offers advantages over traditional chest radiography (6). LUS can accurately and reliably diagnose transient tachypnea of the newborn (TTN) and has a great value in differentiating TTN from respiratory distress syndrome (RDS) (7). Additionally, many of the other common pulmonary and pleural diseases in neonates display specific findings on LUS which can be useful in the differential diagnosis (8).
We developed a screening model of bedside lung ultrasound assessment for infants requiring respiratory support5. Like any other diagnostic technique it should be only used in integration with the clinical assessment and interpreted according to the clinical presentation of the individual patient while considering particular limitations of this modality.
Point of care intestinal ultrasound:
Necrotising enterocolitis is a serious disorder in infants and commonly associated with complications like short bowel syndrome and total parenteral nutrition related issues. The reported mortality is up to 40%, so early diagnosis and management are essential (9). The radiographic diagnosis by XR after clinical suspicion is still the standard in most centers. The main issue with radiograph is being limited to 3 main findings, pneumatosis intestinalis (PI), portal vein gases (PVG), and perforation, and radiograph diagnosis of PI and PVG is sometimes a challenge with low sensitivity and wide range of inter-observer variability. There has been increasing evidence that with real-time ultrasound, PI and PVG can be better detected than with x-ray (10). Ultrasound is able to assess the bowel wall directly and detect bowel wall thickening or thinning, reduced peristalsis or abnormal bowel wall perfusion by color Doppler. Peritoneal fluid, both intraluminal and extra luminal is also visible (11,12). This can be performed in any suspected case with compromised intestinal performance like intestinal obstruction or ischemia and not only in cases with suspected NEC.
Table 1: different applications performed by either professional sonographer (radiologist or cardiologist) or a trained clinician
emergency assessment of suspected hemorrhage
Doppler assessment of cerebral arteries in cases hemodynamic instability e.g. PDA
Intestinal ultrasound Urgent evaluation of suspected necrotizing entercolitis, intestinal ischemia
Lung ultrasound New emerging modality for assessment of common neonatal lung diseases, e.g. RDS, TTN, meconium, pneumothorax, pleural effusions.
Focused heart ultrasound Assessment of specific neonatal hemodynamics issues
Vascular assessment Blood flow by Doppler for assessment of resistance or shunting of blood through arteriovenous malformation or PDA
Interventional POCUS Central line placement, lumber puncture, bladder tapping for urine sample. Peritoneal and pericardial tap of significant effusions
1. Evans N, Gournay V, Cabanas F, et al. Point-of-care ultrasound in the neonatal intensive care unit: international perspectives. Semin Fetal Neonatal Med. 2011;16(1):61-68. doi:10.1016/j.siny.2010.06.005.
2. Pereda M a., Chavez M a., Hooper-Miele CC, et al. Lung ultrasound for the diagnosis of Pneumonia in Children: A Meta-analysis. Pediatrics. 2015;135(4):714-722. doi:10.1542/peds.2014-2833.
3. Escourrou G, De Luca D. Lung ultrasound decreased radiation exposure in preterm infants in a neonatal intensive care unit. Acta Paediatr. 2016:n/a-n/a. doi:10.1111/apa.13369.
4. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-591. doi:10.1007/s00134-012-2513-4.
5. Elsayed Y, Abdelmawla M, Narvey M. A model of integrated lung and focused heart ultrasound as a new screening examination in infants at risk of respiratory or hemodynamic compromise. 2017;6(1):1-14. doi:10.7363/060131.
6. Xirouchaki N, Magkanas E, Vaporidi K, et al. Lung ultrasound in critically ill patients: comparison with bedside chest radiography. Intensive Care Med. 2011;37(9):1488-1493. doi:10.1007/s00134-011-2317-y.
7. Liu J, Cao H-Y, Wang X-L, Xiao L-J. The significance and the necessity of routinely performing lung ultrasound in the neonatal intensive care units. J Matern Neonatal Med. 2016;7058(March):1-6. doi:10.3109/14767058.2016.1152577.
8. Copetti R, Cattarossi L. Lung Ultrasound in Newborns, Infants, and Children. 2011:241-245. doi:10.1007/978-3-642-21247-5.
9. Dilli D, Suna Oğuz S, Erol R, Ozkan-Ulu H, Dumanlı H, Dilmen U. Does abdominal sonography provide additional information over abdominal plain radiography for diagnosis of necrotizing enterocolitis in neonates? Pediatr Surg Int. 2011;27(3):321-327. doi:10.1007/s00383-010-2737-8.
10. Bohnhorst B. Usefulness of abdominal ultrasound in diagnosing necrotising enterocolitis. Arch Dis Child Fetal Neonatal Ed. 2013;98:F445-50. doi:10.1136/archdischild-2012-302848.
11. Gale HI, Gee MS, Westra SJ, Nimkin K. Abdominal ultrasonography of the pediatric gastrointestinal tract. World J Radiol. 2016;8(7):656. doi:10.4329/wjr.v8.i7.656.
12. Kim H-Y, Kim I-O, Kim WS, Kang GH. Bowel sonography in sepsis with pathological correlation: an experimental study. Pediatr Radiol. 2011;41(2):237-243. doi:10.1007/s00247-010-1806-4.
Welcome to the home page for our Integrated Evaluation of Hemodynamics program at the University of Manitoba. This program began in Winnipeg, Manitoba, Canada in 2014 and has been growing ever since.
What is considered normal hemodynamics?
1. Intact or normal hemodynamics implies blood flow that provides adequate oxygen and nutrient delivery to the tissues.
2. Blood flow varies with vascular resistance and cardiac function; both may be reflected in blood pressure(2). Normal cardiovascular dynamics should be considered within the context of global hemodynamic function, with the aim of achieving normal oxygen delivery and end organ performance
3. The current routine assessment of hemodynamics in sick preterm and term infants is based on incomplete information. We have addressed this by adopting an approach utilizing objective techniques, namely integrating targeted neonatal echocardiography (TNE) with near-infrared spectroscopy (NIRS). Implementation of these techniques requires an individual with the requisite TNE training, preferably in an accredited program, who also has a good understanding of perinatal and neonatal cardiovascular, respiratory, and other specific end organ physiology.
Why are premature infants more susceptible to cardiovascular compromise?
Hemodynamic compromise in the early neonatal period is common and may lead to unfavorable neurodevelopmental outcome4. A thorough understanding of the physiology of the cardiovascular system in the preterm infants, influence of antenatal factors, and postnatal adaptation is essential for the management of these infants during the early critical phase5. The impact of the various ventilator modes, the presence of a patent ductus arteriosus (PDA), and systemic inflammation all may affect the hemodynamics6. The poor clinical indicators of systemic perfusion and the relative insensitivity of conventional echocardiographic techniques in assessing myocardial contractility mean that monitoring of the hemodynamics of the preterm infant remains a challenge7.
What is integrated hemodynamics in neonatal care?
Integrated hemodynamics focuses on how to interpret multiple tools of hemodynamics evaluation in sick infants (TNE, clinical details, NIRS, organ specific ultrasound) and the art of formulating a pathophysiologic relevant medical recommendation.
Main objectives of applying Targeted Neonatal Echocardiography and Evaluation of Neonatal hemodynamics
Optimise care of infants with hemodynamic compromise to prevent progression into late irreversible stages of shock (Hypoxia)
Decrease overall PDA related complications (Hypoxemia and hypoxia)
Optimize care of infants with hypoxemic respiratory failure (HRF)
Decrease the incidence of progression of infants with hypoxemic respiratory failure and shock to end organ dysfunction
Objective of the program
Orientation to the hemodynamics concepts and basics
Orientation to the 3 level of the pathophysiologic approach to hemodynamics:
Level one: Relying on blood pressure trends (systole, diastole, and pulse pressure) and waveforms with other clinical parameters (all NICU practitioners)
Level one plus (advanced monitoring): Relying on blood pressure trend and near infrared spectroscopy (NIRS) for assessment of hemodynamics and oxygen extraction (optional to NICU practitioners)
Level two (TNE approach): Relying on both clinical parameters and TNE for objective assessment of cardiac output, extra and intra cardiac shunts, systemic and pulmonary vascular resistance. (Neonatologist trained on TNE)
Level three (integrated evaluation of hemodynamics): integrating blood pressure trends, TNE and NIRS for assessment of oxygen delivery, specific end organ oxygen consumption and the degree of compensation (comprehensive hemodynamic approach)
Understanding the rationale for the measurements and the specific values for each disease, and recognize limitations of the 3 models
To see research that we have done in the area of Integrated Hemodynamics please see our publication list that can be found here.
To access our video series providing examples of TNE and presentations on the use of hemodynamics in clinical application please see our Youtube channel playlist “Integrated Neonatal Hemodynamics”
Wolff CB. Normal cardiac output, oxygen delivery and oxygen extraction. Adv Exp Med Biol. 2008;599:169-182. doi:10.1007/978-0-387-71764-7-23.
Azhan A, Wong FY. Challenges in understanding the impact of blood pressure management on cerebral oxygenation in the preterm brain. Front Physiol. 2012;3 DEC(December):1-8. doi:10.3389/fphys.2012.00471.
de Boode WP. Clinical monitoring of systemic hemodynamics in critically ill newborns. Early Hum Dev. 2010;86(3):137-141. doi:10.1016/j.earlhumdev.2010.01.031.
Sehgal A. Haemodynamically unstable preterm infant: an unresolved management conundrum. Eur J Pediatr. 2011;170(10):1237-1245. doi:10.1007/s00431-011-1435-4.
Vutskits L. Cerebral blood flow in the neonate. Paediatr Anaesth. 2014;24(2):22-29. doi:10.1111/pan.12307.
Noori S, Stavroudis T a, Seri I. Systemic and cerebral hemodynamics during the transitional period after premature birth. Clin Perinatol. 2009;36(4):723-36, v. doi:10.1016/j.clp.2009.07.015.
Elsayed YN, Amer R, Seshia MM. The impact of integrated evaluation of hemodynamics using targeted neonatal echocardiography with indices of tissue oxygenation: a new approach. J Perinatol. 2017. doi:10.1038/jp.2016.257.
Have a look at discharge considerations as that section in the statement speaks to this topic as well!
As bed pressures mount seemingly everywhere and “patient flow” becomes the catch-word of the day, wouldn’t it be nice to manage NAS patients in their homes? In many centres, such patients if hospitalized can take up to 3 weeks on average to discharge home off medications. Although done sporadically in our own centre, the question remains is one approach better than the another? Nothing is ever simple though and no doubt there are many factors to consider depending on where you live and what resources are available to you. Do you have outpatient follow-up at your disposal with practitioners well versed in the symptoms of NAS and moreover know what to do about them? Is there comfort in the first place with sending babies home on an opioid or phenobarbital with potential side effects of sedation and poor feeding? Nonetheless, the temptation to shift therapy from an inpatient to outpatient approach is very tempting.
The Tennessee Experience
Maalouf Fl et al have published an interesting account of the experience with outpatient therapy in their paper Outpatient Pharmacotherapy for Neonatal Abstinence Syndrome. The authors were able to take advantage of the Tennessee Medicaid program using administrative
and vital records data from 2009 to 2011 to capture a cohort of 736 patients who were treated for NAS. Forty five percent or 242 patients were treated as outpatients vs 290 cared for in hospital for the duration of treatment. It is worth mentioning at this point that when the authors say they were cared for as outpatients it really is a hybrid model as the duration of hospitalization for the inpatients was a median of 23 days (IQR 14-35) versus 11 days (IQR 7-18) for inpatients (P < .001). This practice isn’t much different than my own in which I start therapy in hospital and then discharge home with a period of home therapy.
The strength of the study is the volume of patients and the ability to follow-up with these babies for the first 6 months of life to determine what happened to them after discharge. In terms of duration of treatment, the differences are significant but perhaps not surprising. The median length of treatment for outpatients was 60 days (IQR 38-92) compared with 19 days (IQR 10-31) for inpatients (P < .001). What was interesting as well is that 82% of babies were discharged home on phenobarbital and 9.1% on methadone and 7.4% with both. A very small minority was discharged home on something else such as morphine or clonidine. That there was a tripling of medication wean is not surprising as once the patients are out of the watchful eye of the medical team in hospital it is likely that practitioners would use a very slow wean out of hospital to minimize the risk of withdrawal.
An Unintended Consequence
This study found a statistically significant increase in risk for presenting to the emergency department for those patients treated as outpatients.
What this graph demonstrates is that there was no increase risk in the first month but there was for the first 6 months. Despite the increased risk of presentation to the ED the rate of hospitalization was not different. Drilling down the data further, the reason for coming to the ED was not for withdrawal which was 10% in the outpatient and 11% in the inpatient group. The other major reason was The most common diagnoses were upper respiratory infections; 80% outpatient vs 71% inpatient. So while there was a significant difference (which was not by much) my take on it is that it was most likely by chance as I can’t think of how infections in the first 6 months could be linked to choice of medication wean.
What about phenobarbital?
Phenobarbital has been used for many years in Neonatology for control of seizures, sedation (taking advantage of a side effect) and management of NAS. The problem with a median use of phenobarbital for 2 months is its potential to affect development.
An animal study by Diaz in 1999 in which rat pups were given two weeks of phenobarbital starting on day 5 of life and then euthanized demonstrated the following weight reductions when high dose phenobarbital was utilized. In human data, children with febrile seizures treated with phenobarbital in the paper Late cognitive effects of early treatment with phenobarbital. had decreased intelligence than those not exposed to phenobarbital.
The issue here for me is not necessarily whether babies can be treated successfully as outpatients for NAS. The concern is at what cost if the choice of drug is phenobarbital. The reason phenobarbital was chosen is likely due to compliance. We know that the more frequently a drug is dose the less likely compliance will be achieved. Phenobarbital being dosed either q12h or q24h is an ideal drug from a compliance point of view but the ramifications of this treatment deserve reconsideration.
I look forward to seeing further studies on this topic and hope that we see the results of an opioid outpatient treatment program. I know these exist and would welcome any information you as the readers of this blog can offer. Treating patients in the home makes great sense to me but we need to do it with the right drugs!
Much has been written about methylxanthines over the years with the main questions initially being, “should we use them?”, “how big a dose should we use” and of course “theophylline vs caffeine”. At least in our units and in most others I know of caffeine seems to reign supreme and while there remains some discussion about whether dosing for maintenance of 2.5 -5 mg/kg/d of caffeine base or 5 – 10 mg/kg/d is the right way to go I think most favour the lower dose. We also know from the CAP study that not only does caffeine work to treat apnea of prematurity but it also appears to reduce the risk of BPD, PDA and duration of oxygen therapy to name a few benefits. Although initially promising as providing a benefit by improving neurodevelopmental outcomes in those who received it, by 5 and 11 years these benefits seem to disappear with only mild motor differences being seen.
Turning to a new question
The new query though is how long to treat? Many units will typically stop caffeine somewhere between 33-35 weeks PMA on the grounds that most babies by then should have outgrown their irregular respiration patterns and have enough pulmonary reserve to withstand a little periodic breathing. Certainly there are those who prove that they truly still need their caffeine and on occasion I have sent some babies home with caffeine when they are fully fed and otherwise able to go home but just can’t seem to stabilize their breathing enough to be off a monitor without caffeine. Then there is also more recent data suggesting that due to intermittent hypoxic episodes in the smallest of infants at term equivalent age, a longer duration of therapy might be advisable for these ELBWs. What really hasn’t been looked at well though is what duration of caffeine might be associated with the best neurodevelopmental outcomes. While I would love to see a prospective study to tackle this question for now we will have to do with one that while retrospective does an admirable job of searching for an answer.
The Calgary Neonatal Group May Have The Answer
Lodha A et al recently published the paper Does duration of caffeine therapy in preterm infants born ≤1250 g at birth influence neurodevelopmental (ND) outcomes at 3 years of
age? This retrospective study looked at infants under 1250g at birth who were treated within one week of age with caffeine and divided them into three categories based on duration of caffeine therapy. The groups were as follows, early cessation of caffeine ≤ 14 days (ECC), intermediate cessation of caffeine 15–30 days (ICC), and late cessation of
caffeine >30 days (LCC). In total there were 508 eligible infants with 448 (88%) seen at 3 years CA at follow-up. ECC (n = 139), ICC (n = 122) and LCC (n = 187). The primary outcome here was ND at 3 years of age while a host of secondary outcomes were also examined such as RDS, PDA, BPD, ROP as typical morbidities. It made sense to look at these since provision of caffeine had previously been shown to modify such outcomes.
Did they find a benefit?
Sadly there did not appear to be any benefit regardless of which group infants fell in with respect to duration of caffeine when it came to ND. When looking at secondary outcomes there were a few key differences found which favoured the ICC group. These infants had the lowest days of supplemental oxygen, hospital stay ROP and total days of ventilation. This middle group also had a median GA 1 week older at 27 weeks than the other two groups. The authors however did a logistic regression and ruled out the improvement based on the advanced GA. The group with the lowest use of caffeine had higher number of days on supplemental oxygen and higher days of ventilation on average than the middle but not the high caffeine group. It is tempting to blame the result for the longer caffeine group on these being babies that were just sicker and therefore needed caffeine longer. On the other hand the babies that were treated with caffeine for less than two weeks appear to have likely needed it longer as they needed longer durations of oxygen and were ventilated longer so perhaps were under treated. What is fair to say though is that the short and long groups having longer median days of ventilation were more likey to have morbidities associated with that being worse ROP and need for O2. In short they likely had more lung damage. What is really puzzling to me is that with a median GA of 27-28 weeks some of these kids were off caffeine before 30 weeks PMA and in the middle group for the most part before 32 weeks! If they were in need of O2 and ventilation for at least two weeks maybe they needed more caffeine or perhaps the babies in these groups were just less sick?
What is missing?
There is another potential answer to why the middle group did the best. In the methods section the authors acknowledge that for each infant caffeine was loaded at 10 mg/kg/d. What we don’t know though is what the cumulative dose was for the different groups. The range of dosing was from 2.5-5 mg/kg/d for maintenance. Lets say there was an over representation of babies on 2.5 mg/kg/d in the short and long duration groups compared to the middle group. Could this actually be the reason behind the difference in outcomes? If for example the dosing on average was lower in these two groups might it be that with less respiratory drive the babies in those groups needed faster ventilator rates with longer durations of support leading to more lung damage and with it the rest of the morbidities that followed?
It would be interesting to see such data to determine if the two groups were indeed dosed on average lower by looking at median doses and total cumulative doses including miniloads along the way. We know that duration may need to be prolonged in some patients but we also know that dose matters and without knowing this piece of information it is tough to come to a conclusion about how long exactly to treat.
What this study does though is beg for a prospective study to determine when one should stop caffeine as that answer eludes us!