Research: Disruptions in the development of feeding for infants with congenital heart disease

Jones CE, Desai H, Fogel JL, et al  (2020). Disruptions in the development of feeding for infants with congenital heart disease. Cardiology in the Young, 1-8

This just published manuscript is a valuable resource for therapists supporting feeding/swallowing for infants with CHD.  The authors include in the-trenches pediatric therapists from leading programs across the US. It will inform your practice,  whether you are in the hospital, Early Intervention  or community programs that support these complex infants.

The introduction:

Congenital heart disease (CHD) is the most common birth defect for infants born in the United
States, with approximately 36,000 affected infants born annually. While mortality rates for
children with CHD have significantly declined, there is a growing population of individuals with
CHD living into adulthood prompting the need to optimize long-term development and quality
of life. For infants with CHD, pre- and post-surgery, there is an increased risk of developmental
challenges and feeding difficulties. Feeding challenges carry profound implications for the quality
of life for individuals with CHD and their families as they impact short- and long-term neurodevelopment related to growth and nutrition, sensory regulation, and social-emotional
bonding with parents and other caregivers. Oral feeding challenges in children with CHD
are often the result of medical complications, delayed transition to oral feeding, reduced stamina,
oral feeding refusal, developmental delay, and consequences of the overwhelming intensive
care unit (ICU) environment. This article aims to characterize the disruptions in feeding
development for infants with CHD and describe neurodevelopmental factors that may contribute
to short- and long-term oral feeding difficulties. 

They discuss the impact of: cardiac physiology, necrotizing enterocolitis, gastroesophageal reflux, timing of cardiac surgical interventions, sedation and medication, chylous pleural effusion, respiratory support, neurodevelopment, genetic syndromes, a noxious feeding environment, nerve paralysis/paresis, and dysphagia. They then discuss the consequences of these feeding challenges, including: nutritional interference, breastfeeding difficulty, tube feeding, oral aversion, and finally long-term feeding outcomes.

 

Happy Thanksgiving from Catherine Shaker

As the holidays approach, I hope that you and your loved ones are healthy and safe during this difficult and uncertain time. It is a time to be grateful for our many blessings, spend time with loved ones, and look ahead to the new year around the corner.

My goal is to assure that you receive the highest quality continuing education that you trust me to provide.  To this end, my current focus is on expanding, updating and adding even more evidence-base to each of my seminars. As a life-long learner, it has been fulfilling and a labor of love.  In these new 2021 versions of each seminar, you will find new resources, new topics of discussion and the most current evidence-base to inform your clinical practice.

The Covid-19 trajectory remains uncertain. My “Seminar Schedule” TAB lists my planned sites for 2021. As my on-site schedule evolves or should any CEU offerings be offered in a live virtual environment, I’ll update my website, so you can plan.

You can also sign up for my blog postings in order to receive future updates.

Please, as always, reach out  with any questions. Thank you for being part of our community and choosing Shaker Seminars for your professional development.

I look forward to learning along with you soon!

Happy Thanksgiving to you and yours.

Problem-Solving: A Feeding “Window” for NICU Infants?

QUESTION:

There is this idea of a feeding “window” for the infants in our NICU, where PO trials ideally need to happen within this “window” or there could be longer-term feeding issues.  This idea is perpetuated by nurses, physicians, and our developmental care specialist but as an SLP I am not only puzzled but can’t find any research refuting or supporting it. I think the way in which its used by other staff is that this “window” exists around 40-43 weeks and that it is important that if PO hasn’t already happened, that trials at least need to happen during this timeframe.

Does anyone have any research for or against this “window”? Or know the origin of this idea?

ANSWER:

Unfortunately, today many of our preterm infants are being asked to feed much earlier/younger and that can readily cause more stress, unless the approach is infant-guided and not volume-driven. Today, the pressure to get infants out of the NICU often drives many care decisions, especially when it comes to PO feeding.

It’s not uncommon for neonatologists to assume that there is a window within which our preterms must “experience” PO feeding or they will “miss that critical window and never learn”. There needs to be reconsideration of that paradigm to consider instead, individualized readiness to PO. This is why.

That well-intentioned paradigm is based on writings from Gesell back in the 60s that talked about a “critical window” for learning to eat. Those times were different in many ways,  as was the population being described. NICUs were just being developed, there were no therapists as part of the neonatal team, as the need for therapy support, much less feeding support, was not well understood. Many NICU infants did not survive or did so back then with enduring developmental concerns. NICU  infants, though they weren’t asked to PO feed as early back then, they eventfully were PO fed. Prior to initiating  PO, the infants did not have developmental support for the system-based underpinnings to support that future PO feeding and avert maladaptive sensory, sensory-motor and oral-motor patterns that often evolved. At that same time community in Early Intervention, and even in the early 80s when I first started out, we rarely saw former  preemies who had survived the NICU until they were often 4 or 5 years old. Can you even imagine? And they came with horrific stories back then, and complex maladaptive behaviors. The fragile marginal subsystems that underpinned PO feeding had been dormant all that time, and the infants developed maladaptations from motor learning environments that were not therapeutic;  but the nurses in the NICU had done the best they could without therapeutic collaboration/insights, and then parents, after discharge, did the best they could without support of therapists. You can see how “not missing a window” might have been seen as the key, to avert such outcomes, when actually, it was the need to provide the right kind of environment to nurture the prerequisites, individualize care, and then further support emerging PO skills. That was then. This is now.

Today with the advent of neonatal interdisciplinary teams that include PT/OT and ST, we can better support readiness by maintaining those systems for future PO when co-morbidities safely permit. “Readiness” that is not determined based on an arbitrary date or age, but infant-guided readiness based on clinical signs/behaviors in the context of that unique infant’s GA (age at birth) and history/co-morbidities. That is the gestalt  that, when considered thoughtfully,  can set the stage for success, or, if not considered, create the perfect storm for risk. That gestalt benefits from neonatal care that is neuro-protective and promotes positive overcomes and recognizes safety issues inherent with some co-morbidities and clinical presentations that should suggest caution.

Concern for  “missing that critical window” has led perhaps to team decisions to PO with “let’s see what happens” or “let’s let him practice”. But as a thoughtful  nurse once said tome, “why do we ask them to PO when they are not ready? Practice doesn’t make perfect. Practice makes permanent.” I, of course, hugged her!

The concept that preterms must “experience” PO feeding or they will “miss that critical window and never learn” has led to the well-intentioned “pushing PO” and orders to PO on CPAP and HFNC. Many of our former preterms can learn to feed orally at later ages, once weaned in the level of respiratory support, and from my experience, do so with less stress and more safely. Amaizu (2008) reported that gestational age at birth (GA)  influences the ex utero development of oral feeding skills more than PMA (post-menstrual age) at which PO is started. So the age, i.e., PMA (post-menstrual age) at which you start to offer PO is not the key to focus on. It is the bigger picture, which means individualizing readiness considerations.

Advocating for safety for these infants is a critical one for SLPs in the NICU (and PICU). Current NICU technology has advanced to the point that more infants are surviving and yet many are requiring extended periods of CPAP and HFNC. Many extremely preterm infants in our NICU with CLD at post-term (41 weeks PMA +) remain dependent on CPAP or HFNC.  Sadly, this is often the group that gets the most “pressure” to feed and go home.  Does the team ask them to PO feed to not “miss a critical window”? Or does the team maintain their readiness with therapy support, to optimize safety and neuroprotection, by individualizing readiness?

Good collaborative conversations about the benefits of ST being involved to maintain a positive oral-sensory environment, promoting the oral-sensory-motor components that are the underpinnings for future PO feeding, beginning early to foreshadow for parents the swallowing, breathing and postural skills needed, and helping families also support those components, versus attempting PO feeding when the infant is struggling with respiratory stability. Clearly, medical co-morbidities predispose an infant in the NICU to PO feeding problems. Multiple papers have studied that. Those infants with the greatest respiratory comorbidities, often those born < 28 weeks’ gestation and BW < 1000 grams, are most likely to require prolonged NIPPV, CPAP and/or HFNC at those post-menstrual ages when PO feeding is typically attempted. Sick newborns may also present similar issues, secondary to their co-morbidities

If the infant has such respiratory needs that he requires CPAP, or a HFNC, one must ask if PO feeding is really a priority for that infant at that time. The ability to reconfigure the pharynx from a respiratory tract and back to an alimentary tract with precise timing and coordination surrounding each swallow is a concern. When we look objectively in radiology during an instrumental assessment of swallowing physiology, even infants with CLD stable on RA have altered or impaired swallowing physiology as a direct result of their CLD. The bolus mis-direction and resulting aspiration we often observe is typically silent. The need for an “urgent breath” often can predispose an infant with increased work of breathing to silently mis-direct the bolus into the airway during the swallow. The ability of the infant to close the glottis against the driving force of the respiratory support, while breathing with increased effort or with an increased respiratory rate, which effectively creates air hunger, and yet still maintain glottic closure throughout the duration of the swallow, would likely be precarious. Given the infant’s likelihood of baseline tachypnea and increased WOB, the dynamic adjustments of the airway surrounding the swallow are likely to be disrupted and create uncoupling of swallowing and breathing. Indeed, infants for whom we do not necessarily witness aspiration during a dynamic swallow study may indeed show alterations in swallowing physiology that may predispose them to airway invasion under “the right conditions” during PO feeding (changes in nipple flow, changes in position, changes in respiratory support or work of breathing at that moment, for example). The fact that NICU  infants “eat” and “are fed” and “transferred volume” does not equate to “safe or neuroprotective feeding”. Ferrara and colleagues (2017, 2020) and Ferguson (2015) have contributed greatly to our understanding of this risk.

We must of course remember the physiologic stress likely to occur when the infant experiences “feeding” when the infant is not “ready”. It is highly possible the stress of trying to breathe and coordinate a swallow may lay down neural pathways that move the infant away from wanting to eat, by wiring those sensory-motor pathways that lead to current and/or future maladaptive feeding behaviors. We know that studies looking at stress in preterms have shown an association with adverse changes in brain structure on MRIs.

In the NICU seminars I teach, this dilemma is always part of our problem-solving discussions. After 35 years as an NICU SLP,  I so appreciate and always advocate for our key role in dialoguing  with the team, problem-solving and focusing on safety and neuroprotection as the essential part of this practice issue which confronts every neonatal team.

I hope this is helpful.

Catherine

 

Amaizu, N., Shulman, R. J., Schanler, R. J., & Lau, C. (2008). Maturation of oral feeding skills in preterm infants. Acta Paediatrica97(1), 61-67.

Dumpa, V., Kamity, R., Ferrara, L., Akerman, M., & Hanna, N. (2020). The effects of oral feeding while on nasal continuous positive airway pressure (NCPAP) in preterm infants. Journal of Perinatology40(6), 909-915.

Ferguson, N. F., Estis, J., Evans, K., Dagenais, P. A., & VanHangehan, J. (2015). A Retrospective Examination of Prandial Aspiration in Preterm Infants. SIG 13 Perspectives on Swallowing and Swallowing Disorders (Dysphagia), 24(4), 162-174.

Ferrara, L., Bidiwala, A., Sher, I., Pirzada, M., Barlev, D., Islam, S., … & Hanna, N. (2017). Effect of nasal continuous positive airway pressure on the pharyngeal swallow in neonates. Journal of Perinatology37(4), 398.

 

Supporting Feeding for Infants with Cleft Lip/Palate

Congratulations to Brenda Fetter, SLP  from Childrens’ Mercy in Kansas City for joint authorship on a wonderful new publication.

Kaye A, Huff H, Fetter B, Thaete K (2020) Cleft Lip and Palate Newborn Care and Feeding: A Primer for Bedside Nursing Providers. Int J Nurs Health Care, 2 Volume 03; Issue 07

Contributions from a  plastic surgeon and pediatric dietician make it a unique offering. Witten as a primer for bedside nursing providers working with newborns with cleft lip and palate, it provides excellent information for  all of us to consider for informing our practice with this infant population.

While each of us may have a slightly different slant on intervention approaches based on our unique clinical experiences, it provides a solid compendium of information to inform our practice.

 

Click on this  secure link for the open access article:  Kaye et al (2020) cleft palate primer for RNs

The Science of Breastfeeding

The science and physiology of breastfeeding has always been a great interest of mine. Partnering with IBCLCs early on taught me so much. They instilled in me a desire to learn and understand the critical implications for our bottle-feeding practice with infants, especially with my work supporting preterm infants and their mothers in the NICU. The works of Paula Meier (regarding the infant-controlled flow rate at the breast — -once mother pumps through letdown—and how it reminds us then to offer a slow  controlled flow from a man-made rubber nipple, to minimize adaptation required and optimize safety). The works of Nyqvist about successful breastfeeding experiences as early as 29 weeks PMA (I suspect likely related to controlled flow rate that absolutely best supports breathing stability for suck-swallow-breathe synchrony). With every mother in our NICU that I am blessed to work with via consult regarding bottle-feeding, if mother is pumping, I advocate for early nuzzling, early breastfeeding, and share the research (in a simple way) about flow rate, how breastfeeding is actually easier than bottle feeding for preterm infants, and that breastfeeding always facilitates progression of bottle feeding skills  (in my experience). The infant-guided nature of breastfeeding that supports the “dance” between mother and infant is at the heart of trust, communication and trauma-informed neuroprotective care.

Too often I hear well-intentioned caregivers in the NICU tell mothers that breastfeeding is harder for preemies, and I see the sadness come over the mother. I am always so grateful to be there to gently reinforce what the evidence tells us and encourage our mothers on behalf of our infants.

I can’t imagine working with bottle-feeding infants without understanding the science and physiology of breastfeeding. In every course I teach we carve out time to discuss the science and physiology of breastfeeding and how we can best support bottle-feeding experiences that facilitate continued successful breastfeeding.

Problem-Solving: Thickening Breastmilk Post Swallow Study

QUESTION

I have been out of the pediatric feeding and swallowing world for several years now. I had a friend reach out that has a seven-week-old infant with dysphagia. She noticed her baby was having increased strider and apneic spells during breast-feeding. She recently had an MBS completed and was placed on mild nectar thick liquids (she may have been told 1/2 nectar??). They also recommended a Dr. Brown’s bottle with a level two nipple. They recommended she use a specific thickener for breast milk; however, it is currently on back order. Does anyone have different suggestions for how to safely thicken breast milk utilizing a thickener that is approved for infants? Any information is appreciated!

ANSWER:

An easy answer would be to suggest Gel Mix, known to thicken breastmilk.

But a simple answer may not be best.

Because I tend to appreciate the history and co-morbidities to form my data set, and then add clinical data to make recommendations, it is challenging to make a suggestion that I have confidence in, since all thickeners, as you know, are not created equal nor equally suited for every infant nor is aspiration just “aspiration”.

The challenge is suggesting an alternative thickener that wasn’t objectified under fluoroscopy, as that can perhaps create more risk than anticipated. Because the SLP had the opportunity to objectify the impact of that level of thickening and that thickener, and that specific nipple, (as well as others, I suspect), then someone else changing the “prescription” may not be optimal.

Has mother contacted the SLP who did the VFSS for guidance as to optimal alternative plan in the interim, until prescribed thickener is available? That SLP will likely be best able to minimize the risk, given her understanding of the infant’s swallowing physiology, access to full data set and understanding of what would be indeed contraindicated. Not knowing etiology for the aspiration, i.e. pathophysiology, also whether the events were silent, and the etiology for the stridor, and what other interventions appeared to increase the safety margin (versus degrade it) such as co-regulated pacing or resting. I would be remiss to not refer her back to that SLP for next steps.

I am curious if infant has also been a bottle feeder too, prior to the VFSS or if the VFSS as her first PO trial with a bottle; if not, that might an add artifact. Wonder what thickener was suggested. EBM is super thin liquid so often doesn’t require a flow rate as fast as a level 2 for the mild amount of thickener as described. Wonder if EER (extra esophageal reflux) has altered laryngeal/tracheal sensation.

Also take a look at this article from the team at Boston Children’s, which summarizes  the most current evidence-base regarding thickening in pediatrics: Duncan, D. R., Larson, K., & Rosen, R. L. (2019). Clinical Aspects of Thickeners for Pediatric Gastroesophageal Reflux and Oropharyngeal Dysphagia. Current gastroenterology reports, 21(7), 30.

I hope this is helpful.

Problem-Solving: Bradycardia in the NICU

Question:

We currently have a former 33 week twin, now 36 and 4 weeks who frequently demonstrates bradycardia events but only during feeding attempts. He does not drop is oxygen saturation at all, in fact this almost always remains at 100% during feeding. His drop in heart rate is usually brief but this is usually after being stimulated. He wakes up consistently for feeding, shows appropriate feeding readiness cues, has a very strong non nutritive suck pattern. With bottle feeding attempts he demonstrates a very poor suck/swallow/breath sequence. He was initially on the ultra preemie nipple to slow the flow down to assist with coordination, however would demonstrate a very fast rate of suck, inefficient with fluid expression with suspected oral pooling in the posterior oral cavity prior to swallow. We have trialed a preemie nipple but without much change in his pattern with the goal of trying to achieve a more functional suck to swallow ratio. I do feel his swallow response is delayed post suck and inconsistent throughout the feed depending on alertness. Could these frequent bradycardia events be a vagal response? As a result of aspiration? Any positioning or flow rate recommendations to trial instead? You can very much tell when he is going to drop his heart rate during a feeding, and usually with re-positioning, taking a break from the feeding it can be prevented but I’m still curious as to a possible etiology for this. He is still currently on caffeine due to these frequent events. Any insight appreciated.

Answer:

This is a challenging clinical presentation to problem-solve but not an uncommon one in the NICU.

Can you tell us any more about the infant’s history  and co-morbidities (especially respiratory, neurologic, GI, postural/sensory-motor?) is he otherwise progressing as one would expect of a former 33 weeker now 36+ weeks PMA?

Bradycardia events during PO feeding can occur at 36 weeks PMA but such are not typical of preemies at that age and are unlikely therefore to be “a variant” of prematurity itself. Some bradycardic events during PO occur without co-occurring desaturation, especially if the bradycardic events are not prolonged. However, the provoking of a bradycardia when the infant  PO feeds  is worrisome none the less. Bradycardia in NICU infants during PO was correlated with aspiration in a study/paper by Neina Ferguson in 2015.

When I think about a differential as to about what co-morbidities might provoke such episodes at 36+ weeks, what comes to mind includes : GI (e.g., EER/LPR), respiratory (swallow-breathe incoordination leading to uncoupling of the swallow -breathe interface secondary to increased WOB, intermittent tachypnea). Both may present a pathway to airway invasion. In addition, alterations in neural integrity (which can occur in a former 33 weeker but are less likely to be the sources of provocation than the other two possibilities I mentioned). There can also be caregiver artifact (i.e., not recognizing and/or responding to infant’s physiological communication and/or swallowing behaviors from moment to moment , to contingently titrate interventions to avert decompensation; using  a flow rate that is too fast, well-intentioned prodding). The last possibility, caregiver artifact, seems unlikely given that he is having these events with you, not only with, for example, parents or staff. But some added interventions might help; more on that later.

Your clinical description suggests a prolonged sucking pattern, likely in the setting of increased WOB and intermittent tachypnea. An increase in WOB may be [resent at baseline or can be recruited (or exacerbated)  by a strong continuous sucking effort, without timely and sufficient breaths. This can lead to the need for an urgent breath, even with flow rate control via Dr. Brown’s premie or ultrapremie nipples. Bolus sizes beyond the infant’s capacity can then perhaps “overwhelm” the required dynamic adjustments of his airway that need to surround the swallow. This may lead to a clinical impression of a delay in onset of post-swallow breath (due to the infant’s attempt to prolonged airway closure as a means to protect the airway). Along the swallow pathway, the infant may attempt adaptations that, unfortunately, create resulting maladaptations that lead to further risk for laryngeal penetration and/or aspiration.

In my clinical experience, bradycardia during PO at 36 weeks PMA, even with interventions in place, is most often correlated with airway invasion. A vagal response can indeed result in bradycardia but is often seen as a maturational variant, again unlikely at 36 weeks PMA. Polyvagal Theory, which is quite complex, postulates and describes the fragile nature of CN X function related to prematurity.

When fluid approaches the airway of a preterm infant, there is a reflex that is supposed to be elicited to close the airway; however, its timeliness, consistency of provocation and effectiveness are not well understood. Caffeine prescribed to stimulate HR as you describe can have the unintended sequelae of increasing EER//LPR, so EER/LPR could still be part of the differential too.

Without knowing any more about the infant’s history and co-morbidities, I would suggest you continue to contingently rest the infant, use controlled flow rate to limit bolus size, and, if you have not trialed it yet, use elongated swaddled sidelying (to optimize tidal volume and respiratory reserves). Then incorporate contingent co-regulated pacing based on the infants communication and swallowing behaviors. If,  with these interventions, you cannot avert the events described, I would instrumentally assess swallowing physiology to help elucidate the etiology(ies) for the events, and the effect of further titrated interventions (frequency of pacing, flow rate). Unfortunately, some of our preterms who have adverse overt events during PO feeding are also observed to silently invade their airway under fluoroscopy.

I hope this is helpful.

Follow-up Question:

What does WOB stand for?

Follow-up Answer:

Sorry for the acronym. I hear the term (and see it in real life) so often in the NICU and PICU that it is just part of my vocabulary.

WOB stands for “work of breathing”, which often adult RNs refer to as shortness of breath (SOB). In the preterm population, increased WOB refers to the extra muscular effort utilized to “move air” or to compensate for the difficulty moving air. It may include during feeding typically chin tugging, shoulder girdle hiking, nasal flaring/blanching, and retractions (pharyngeal, suprasternal, supraclavicular). This “work”, combined with an elevated shallow respiratory rate, can render the  swallow-breathe interface precarious. When you work out at your max effort on a treadmill, you would (or should!) recruit all of these compensatory behaviors to get you through the task (your workout). That’s one of the reasons why even skilled athletes rarely if ever drink from their water bottle at high levels of aerobic activity/demand.

Preterm infants have musculoskeletal immaturity, and so they often have to resort to working harder to move air, even at rest. So they often start with an already increased level of respiratory effort at baseline. Because PO  feeding is their “aerobic exercise” (their heart and lungs work harder during PO feeding) they unfortunately often need to further increase their WOB to accommodate. This creates risk for airway invasion and requires the caregiver to have watchful vigilance during PO feeding. The caregiver needs to carefully watch for changes in WOB and related swallowing behaviors that may suggest swallowing and breathing are becoming uncoupled, and carefully titrate interventions to support the underpinnings for coordination.

Thanks for asking for clarification.

Research: Feeding outcomes in former preterms in the first 7 months of life

Click on this secure  link: Hill et la (2020) Bottle Feeding preterm Infant first 7 months of life

Those of you in Early Intervention and in the NICU will find this new paper just published a valuable addition to your research base for practice.

Hill, R. R., Park, J., & Pados, B. F. (2020). Bottle-Feeding Challenges in Preterm-Born Infants in the First 7 Months of Life. Global Pediatric Health7, 2333794X20952688

It reinforces some of the key factors that may lead to enduring feeding problems after the NICU. It may be helpful for your neonatology team, as its findings suggests that watchful vigilance both in the NICU by the SLP, and indeed after discharge by our colleagues in Early Intervention,  should be a part of the plan of care for our at risk infants and their families. Perhaps this early provision of infant-guided support may in the long run avoid the onset of feeding aversions that can arise from stressful feeding experiences.

Quoting their conclusions:

Very preterm infants (i.e., those born <32 weeks GA at birth) had significantly more symptoms of problematic bottle-feeding than infants born full-term, moderately preterm or late preterm. Factors such as BPD (Chronic Lung Disease), GER, and congenital anomalies of the face, mouth and gastrointestinal tract were significant contributors. Early difficulty with breastfeeding was also a risk factor for later difficulties with bottle-feeding. There was improvement in symptoms with increasing age, which is likely reflection of improvement of medical factors and infant maturation. These findings support the need for frequent assessment of feeding in preterm-born infants after NICU discharge and provides clinicians with information regarding particular medical factors that place infant at risk for feeding difficulty beyond the NICU. The identification of infants who are struggling with bottle-feeding may facilitate interventions within the primary care setting or referral to feeding experts to improve longer outcomes and decrease the likelihood of negative sequelae that could persist into late childhood.

 

 

Research: Videofluoroscopic swallow-study outcomes among infants with tracheotomies

While problem-solving a recent NICU infant I was following with a tracheotomy, I incorporated this information from a study done through Nemours Childrens Hospital in DE. It was presented as a poster session at the ASHA convention, and has not been published to my knowledge. The study was well-done, the findings are informative and can help guide our care of infants in the NICU who require tracheostomy. Contact the authors for more information. I am quoting below from the poster presented.

Videofluoroscopic swallow-study outcomes among infants with tracheotomies                        Jeannine Hoch, MA, CCC-SLP; Michele Morrow, MS, CCC-SLP; Heather Keskeny, MA, CCC-SLP; Aaron Chidekel, MD   

Due to advances in technology, tracheotomy tube-placement is becoming increasingly common during the first year of life.

Infants with tracheotomy are at risk for developing feeding and swallowing problems: There is a paucity of descriptive information regarding dysphagia for infants following tracheotomy. Lack of available research leaves many clinicians feeling unprepared to provide services for pediatric tracheotomy patients.

Infant feeding patterns may also be impacted by environmental and associated medical conditions such as: Gastroesophageal reflux, Low birth-weight, Bronchopulmonary dysplasia, Long-term nasogastric tube-feedings, disruption of parent–infant interaction due to long-term hospitalization

Goals of their study:

  • Based on reports from videofluoroscopic swallowing studies, what are the swallow characteristics of infants with tracheotomies?
  • What percentage of patients required enteral feedings via nasogastric and/or gastrostomy tube-feedings?
  • Are trends present between swallow dysfunction, underlying medical conditions (gastroesophageal reflux, premature birth, nature of illness necessitating tracheotomy tube placement), and the need for enteral feedings?

A Retrospective study

  • Subjects (n = 27) whose Tracheotomy-tube placement by 4 months of age with mechanical ventilation  – Males (n = 16), Females (n = 11) – Exclusion criteria included grade III or IV IVH or presence of severe neurodevelopmental delays that preclude initiation of oral feeding
  • Data collection:  Medical history, Results of initial videofluoroscopic swallow-study, Results of serial follow-up studies when applicable

Data analysis

  • Trends may exist between initial swallow-study findings and reason for tracheotomy-tube placement:
    • Airway issues (n = 10): delayed swallow-initiation (80%), laryngeal penetration (80%), aspiration (50%), residue following swallows (50%), and nasopharyngeal reflux (50%)
    • Respiratory distress with BPD (n = 17): delayed swallow-initiation (53%), laryngeal penetration (71%), aspiration (29%), residue following swallows (47%), and nasopharyngeal reflux (41%)
  • Among patients who underwent G-tube placement (n = 17):
    • Less than half (47%) had documented aspiration on their initial swallow-study.
    • Majority (94%) had documented reflux.
  • Among patients who underwent follow-up swallow studies (n = 17):
    • Laryngeal penetration tended to persist (n = 6) more frequently than it resolved (n = 4).
    • Aspiration tended to resolve (n = 5) more frequently than it persisted (n = 2).
  • Report of oral motor-impairment (n = 12, 44%) and oral phase-impairment (n=17, 63%) was common.
  • All of the patients (n = 27) achieved at least partial or therapeutic oral-feedings as noted on recommendations from their final swallow-study.

 

Problem-Solving: Onset of severe oral aversion in the NICU

Question:

I currently have an infant who has low tone with severe oral aversion impacting P.O feeding. The infant was previous a great feeder but needed to be intubated. Since then, the nursing staff reported poor feeding skills, and I noted poor tolerance of positive tactile stimuli to her checks and non-nutritive sucking for calming. I was wondering if you have any strategies to improve the tolerance of oral stimuli when an infant has an aversion combined with low tone.

Answer:

Will share some thoughts and also some questions. My mind starts right away asking questions to help me start a “differential” as one of neonatology colleagues taught me many years ago. I am so grateful that she took the time to help me problem-solve in a way that physicians are taught. It has really helped me dialogue with the neonatologists.

What is the etiology for the hypotonia? Is this a former preterm or a sick newborn and what are the co-morbidities that would lead to the need for interval intubation? The bigger picture is likely relevant to sorting this out. Why was she recently intubated? It is uncommon for brief interval intubation to completely “change” the oral sensory system. Maybe it isn’t the intubation that is causal but co-occurring events such as the pressure to “get back to PO” ?  or co-morbidity-related? Could this be r/t well-intentioned pushing to feed post extubation? How is she being fed now? “PO all” attempts despite adverse responses? Depending on how volume driven versus infant-guided your unit is, that may be adding fuel to the fire. Are they still trying to PO? I wonder if any of her maladaptive behaviors started as adaptive behaviors (i.e., not wanting to PO d/t breathing too fast at that moment, flow rate too fast, fluid moving toward the airway) unbeknownst to the caregiver feeding her…? Infants do things for a reason as you know and it is often physiologic, so looking from that perspective always informs us.

I wonder if being a “great feeder” for the nurses was a volume-related commentary versus one reflecting quality of feeding? maybe there have been qualitative issues all along that were not apparent.

If she is currently PO, I’d want to just be present when RN feeds and learn along with the infant and nurse about the feeding relationship with the caregiver to help inform your differential. May need a true break from PO, such that for now PO only with a therapist (to reset her sensory system and then attempt to progress back to infant-guided positive PO feeding from a better baseline of oral-sensory readiness).

Will she accept her own hands to face in a swaddled side lying position, ensuring WOB is not problematic? I’d start there as it’s likely tolerated best, and you can facilitate firm deep pressure (versus light touch, which may be processed as more averse). Look at her big picture as the foundational data set. Then listen to the infant. She can likely tell us the “why” or at least lead us in the right direction.

Hope this helps.

Catherine

Research: Challenges to eating, swallowing, and aerodigestive functions in infants

Jadcherla, S. R. (2019). Challenges to eating, swallowing, and aerodigestive functions in infants: a burning platform that needs attention! The Journal of pediatrics211, 7-9.

Always insightful and leading-edge, Dr. Jadcherla at Nationwide Children’s clearly identifies major focus points  in our journey toward supporting independent functional feeding for all of our pediatric patients. Follow his research in those key areas. Read the entire paper on Google Scholar.

Quoting from the article:

“…only when we understand the causal and ameliorating mechanisms of eating, swallowing, and aerodigestive dysfunctions, and the cause for practice and process variation, will we then be able to modify strategies for appropriate diagnostic, therapeutic, and rehabilitative approaches to ensure safe feeding during and beyond ICU stay, lest, we run the risk of over- or underutilization of gastrostomy procedures. In the end, we seek to restore the most fundamental of human behaviors, safe eating”

 

Quoting from the article:

“Summary of 10 Ps That Require Careful Attention to Disrupt the Rising Prevalence of Pediatric Dysphagia

 (1) Physiology of eating, swallowing, and aerodigestive functions in the context of the developing infant must be better understood. Maturational variability and rapid growth during early infancy offer a unique opportunity to improve eating patterns in premature infants.

 (2) Pathophysiology of the mechanisms of pediatric dysphagia also requires careful study so as to provide pathophysiology-guided clinical care.

 (3) Patient characteristics are variable in any given scenario of feeding difficulties, and attention to the risk factors is key because modification of risk factors can improve outcomes.

 (4) Parent involvement and anticipatory guidance for dealing with eating difficulties, swallowing, and aerodigestive morbidities must be undertaken from early on, so that appropriate and timely interventions can be addressed.

 (5) Providers in the healthcare system may be unaware of the factors that influence infant feeding, and physicians may wholly delegate this area to occupational therapists or speech language pathologists. Newer data over the last 2 decades has emerged, and the pace of rapid translation from discovery to implementation will be enhanced when silos of expertise are eliminated and knowledge, attitudes, and skills are reexamined.

 (6) Procedures performed in the diagnosis of pediatric dysphagia need standardization, with careful reevaluation of indications and contraindications in the context of the fragile ICU infant. Diagnostic delays lead to delays in timely interventions during critical windows of opportunities.

 (7) Precision medicine is possible only when the underlying mechanisms are understood and targeted with innovative approaches at the bedside of the infant in the ICU.

 (8) Personalization of diagnostic, therapeutic, and rehabilitative approaches in the context of the infant’s condition, maturity, disease, and functional skills is important.

 (9) Pragmatism in approaches coupled with humanism is needed particularly with developing longitudinal follow-up of feeding milestones. Clinically meaningful outcomes such as independent feeding must be a functional goal”

Enjoy this fabulous read!

Pediatric Feeding Disorder (PFD): “More than a symptom, pediatric feeding disorder is its own diagnosis”

Feeding Matters (feedingmatters.org) is the first organization in the world serving kids with pediatric feeding disorder (PFD) developed by mothers and guided by an interdisciplinary team, of professionals across communities to improve the system of care for children with pediatric feeding disorder. Founded in 2006 by mothers of infants and children with persistent all-encompassing feeding problems, it has partnered in the latest developments to advance the research and treatment of pediatric feeding disorder.

Their efforts have now made possible an amazing milestone in the evolution of accessing support for infants and children with feeding problems, and their families.

The U.S. Centers for Disease Control and Prevention (CDC) has officially approved Pediatric Feeding Disorder (PFD) as a diagnostic code (R code) to the International Classification of Disease edition (ICD-11) in October 20201.

This creates a stand-alone diagnosis and definition for PFD to provide common diagnostic criteria to ensure early and accurate diagnosis among clinicians when assessing children with feeding difficulties.

For so many years, pediatric therapists  have been ​advocating little patient by little patient to bring recognition of the need for this stand-alone diagnosis. I remember starting out back in the late 70s when we had no advocacy group like Feeding Matters and the team of experts assembled  to articulate the need and open the doors for so many infants and children in a timely comprehensive way. Mothers especially were often left to feel that “failure to be able to feed” your child was like “failure to be a mother, as one of the founding mothers of Feeding Matters told me years ago.

All of the pediatric clinicians in the trenches, like me,  thank the professional team for the diligence to see this through. And we thank the founding mothers of Feeding Matters who had the courage to advocate and persist in their search for a change, despite such arduous odds.

This successful effort has the potential to change the trajectory of the lives of many infants and children, and their families. We are blessed to be a part of it!

Click on this link for a free download of the seminal article DOI: 10.1097/MPG.0000000000002188).

Click on this link for the Feeding Matters press release:

https://www.feedingmatters.org/pfd-advocacy-in-action-pfd-as-a-stand-alone-diagnosis/?fbclid=IwAR2BAhqXNYGxlMyIz2tB7U19DXH8bb5YfnhlE_Qv0NHbg1P1Qy0HgNMnKUo

Research: Effects of Additives for Reflux Management and Dysphagia Management

This manuscript  was released in 2019. It  is a compelling read about potential adverse effects of cereal thickeners (rice versus oatmeal) added to formula, and adding medications to formula, and their impact on osmolality. Alteration of ready-to-feed preterm formulas may significantly increase osmolality and have unintended consequences (feeding intolerance, pain, prolonged GI transit, bacterial overgrowth).

The AAP has advocated against the use of thickening agents for high risk preterms under 44 weeks PMA. In the NICU and with infants after discharge in general, we always need to take pause prior to thickening feedings for infants with dysphagia, and do so after other interventions are offered (change in nipple flow rate, position, use of pacing strategies). For many infants, implementing these strategies will support safe swallowing. This manuscript adds to our understanding of the importance of considering risk-benefit ratio in all that we do.

The salient findings from this study are:
1) Cereal thickening amounts and agents added to ready-to-feed liquid preterm formulas impact osmolality and can cross the limits of AAP safety thresholds. Specifically, the thickening agent increases osmolality, and oatmeal contributed to greater osmolality compared with rice on an equi-volume basis. 2) Commonly used vitamin and electrolyte supplements added to ready-to-feed preterm formula can remarkably increase osmolality

They conclude: 1) When thickening is still a strong consideration for Dysphagia/GER management, the ready-to-feed thickened formulas may be a safer alternative as the mixture is more homogeneous and has been vigorously tested, and passes FDA regulations including osmolality thresholds. Other alternative treatment strategies may include modifications to nipple flow or feeding volume, pacing while feeding, or appropriate positioning of the infant during feeding.  2) mixing medications in the entire volume of feed, or dividing doses across multiple feeding sessions mixed with feeds to decrease the osmolality as much as possible.

I am attaching this manuscript as it will be a good discussion point with our medical teams in the NICU, with pediatricians and GI specialists, and for those of us who follow infants in the community.

I hope this informs your practice.​

Here is a link to this article. 

Problem-Solving: SLP completing NGT feedings in NICU

QUESTION

Do you as the SLP drop NG feeds when finishing oral feeds and/or treatment sessions instead of the RN? Does your department or hospital have any guidelines for this?

ANSWER

It is understandable that our NICU nurses can get very busy these days with greater numbers of infants to care for, conflicting patient needs at the same time, and time sensitive interventions. While we are there to lend a hand to a change diaper prior to out treatment, warm the formula/milk etc., it sounds as if you are in a situation where what you are being asked to do is making you uncomfortable. Understandably so, from what you have told us. Our tendency to help out if asked is commendable but must be thoughtfully weighed for its risk-benefit ratio to the patient, the hospital, and of course, to us.

In the NICU, placing an NGT, and/or offering that remaining portion of a PO feeding which requires delivery via an NGT feeds are neither without potential risk for adverse events. NICU RNs are required to meet competencies to complete these medical interventions, and trained mentorship, give it is in their scope of practice. Adult RNs who “float” to NICU to help in crisis situations, require competencies as well.

These procedures also are, to my knowledge, not within the scope of practice of the SLP, either by ASHA standards nor by typical hospital job descriptions. Doing so, because of its high risk problem-prone nature in neonates (provoking emesis, provoking bradycardia and/or apnea, co-occurring EER event, incorrect placement  if “dropping NGT – by which I think you are meaning “placing an NGT”. Even delivering the remaining volume in an NGT that is indwelling may lead to an adverse unanticipated event and place the SLP at risk. Working outside our scope of practice may open us up to serious liability issues.

I suggest you take this question/situation to your rehab leader and request input from NICU leadership, and hospital Risk Management. Proactively considering every action we undertake, and its risk (for the infant, for you, for the hospital), is essential in the environment of neonatal intensive care.

I commend you for thoughtfully pursuing this request made to you.

I hope this is helpful.

Problem-Solving: Silent Deep Laryngeal Penetration

QUESTION:

I am a graduate student in my medical externship and I’m trying my best to understand this:

It’s my understanding that the internal branch of the recurrent laryngeal nerve mediates sensation below the vocal folds and mediates a cough reflex. This is why we’d expect a cough if material is sensed below the level of the vocal folds in a pt with an intact cough response. If material gets below the vocal folds and no cough is produced, we call that silent aspiration.

It’s my understanding that the superior branch of the laryngeal nerve mediates sensation above the vocal folds and an expected response to material above the level of the vocal folds is a swallow.

What about material sitting on top of the vocal folds (level 5 of the pen-asp scale)? Is that expected to elicit a cough or a swallow?

If material sitting on top of the vocal folds is considered penetration (because it did not go below the vocal folds) and is expected to elicit a cough, wouldn’t that mean that there is such a thing as silent penetration?

DR. JAMES COYLE’S ANSWER:

Good for you in accurately describing the sensory innervation of the larynx. 

In a healthy state the stimulus of foreign material on the vocal folds should elicit a response of some sort.  However, people who frequently exhibit laryngeal penetration, people who smoke, and people with other conditions that desensitize the mucosal receptors’ or the sensory system’s response to irritation can lead to the need for a higher threshold of stimulation to elicit a response (attenuated response).  So that is why the distinction is important.  “Silent” laryngeal penetration to this level (PAS 5) would be unlikely in a person with intact laryngeal sensation while more likely in these other situations.

Also, it is perfectly normal for material (thin liquid especially) to just barely enter the vestibule and then spontaneously be ejected to the pharynx during laryngeal closure (PAS 2).  So if you wanted to use these terms I suggest including the depth of penetration in the descriptions (as the PAS scores include).  For instance, “silent deep laryngeal penetration” is different from “silent shallow laryngeal penetration” as explained above.

 

CATHERINE’ S FOLLOW-UP COMMENT:

Thank you, Dr. Coyle, as always for your input that informs our practice, whether in pediatrics or adult populations.

This paper below may be of interest to you. While it was published in 2000, it was a study well-done from the team Children’s of Colorado. It remains foundational in the world of pediatric dysphagia. In the setting of particular co-morbidities, especially CLD in our littlest ones, such understanding becomes critical in developing an algorithm for each infant that helps peel apart the likely impact of physiology on risk to invade the airway, not just in the moment in radiology, but in the course of a true feeding,

Friedman, B., & Frazier, J. B. (2000). Deep laryngeal penetration as a predictor of aspiration. Dysphagia, 15(3), 153-158.

Abstract: This study describes the incidence of laryngeal penetration in 125 dysphagic children ranging in age from 7 days to 19 years who were seen over a 6-month period at The Children’s Hospital in Denver, Colorado. Laryngeal penetration was identified in 60% of the study group, with 31% demonstrating deep laryngeal penetration. Of the children exhibiting deep laryngeal penetration, 85% aspirated, suggesting a strong correlation between these two events. It was noted that children exhibiting deep laryngeal penetration often began to aspirate further into their feedings. Use of extended feedings during videofluoroscopy is discussed as a diagnostic strategy in the presence of deep laryngeal penetration.

I hope this is helpful in your key learnings.
Keep up the critical thinking!