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.

 

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.

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

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!

 

Problem-Solving: Impact of High Narrow Palate in the Setting of Tethered Oral Tissues

QUESTION: Infant  diagnosed with a tongue tie at birth. He is now 9 months old. We never clipped his tie, and he is still going strong with breastfeeding .

At birth, told the he has a very high arched palate. My pediatrician brushed it off saying it was fine. The ENT we took him to for the tie also pretty much brushed it off. Same thing. If he was feeding fine, he was probably fine. But when I look into his mouth now, I am shocked by how high his palate is. I have tried to read up and research it, and I have learned that the tongue is responsible for flattening out the palate (so it makes sense that a tongue tie would inhibit this). He is getting to the speaking age, it’s made me question if he really could end up having some speech issues. It seems logical that it would be nearly impossible for him to make palatal sounds when the time comes if he can’t even get his tongue close, but I can’t really find anything out there that gives me guidance.

My questions:
* Does a tongue tie with a high arched palate likely lead to more speech issues than a tongue tie?
* Is there anything to suggest that if I released it now, it would help with palate development? (or is there a point where releasing it would or would not make a difference?)

ANSWER:

Sounds like your little guy is doing well.

A good resource for you would be Lori Overland and Robyn Merkel-Walsh, both SLPs and accessible via ASHA Community. There latest publication is an invaluable resource regarding the potential broad reaching effects on the dynamic oral-motor and oral-sensory synergies that underpin swallowing and speech sound development.

Functional Assessment and Remediation of Tethered Oral Tissues (TOTs) 2018

The dynamic systems are integrated in utero as early as 17 weeks of life, when the fetus has fully formed the aerodigestive system as the fetus swallows amniotic fluid. This sensory- motor learning lays down the motor mapping for feeding in the delivery room with skill and integrity. Alterations, be they structural and/or muscular, likely impact this motor learning and can, even in subtle ways, create differences in how muscle groups function and provide the “forces” , if you will, that then may impact boney relationships, and vice versa. The forces that are brought to bear in utero on the palate do indeed help to shape it in utero.

Infants can learn to compensate with feeding but may also learn maladaptive patterns that yield functional feeding with qualitative differences, especially as more complex oral-motor skills need to emerge for refined chewing. Those qualitative differences may influence motor learning for speech. You are likely already having wonderful opportunities at 9 months to listen for the range of vowel sounds, articulatory contacts during his babbling and sound play and imitation to give you some insights, as to evolution of speech sound learning. As more complex speech sound integration is required for connected speech, you’ll gather more data.

In my practice as an acute care pediatric SLP, and an outpatient pediatric SLP for many years prior, I have worked with many infants and children with apparent tethered oral tissues with various functional presentations. Meaning, some can get by functionally and run under the radar. Others have more overt and sometimes more subtle alterations in function. My background in neurodevelopmental treatment (NDT) in pediatrics really opened my eye to the dynamic systems approach to the postural mechanism, including the oral-motor/oral-pharyngeal components, and the potential far reaching effects of tethered tissue anywhere along the human body.

I hope this is helpful

Problem-Solving: Where to Begin with Former Preemie with Multiple Complex Co-Morbidities

QUESTION

I’m looking for some insight on where to begin with this case:
The child’s age : 4 Months (Preemie Baby – 35 Weeks, will be 5 months June 26th from day he was born)
Aspiration pneumonia, G-Tube and Nissen Fundoplication, nothing by mouth

Issues with swallowing – risk of saliva entering to lungs – can’t give him pacifier, reflux, and unknown genetic abnormality/corpus callosum.

Any help would be appreciated!

ANSWER
Sounds like he is a late preterm  who is going to be 5 months soon, and would then be not quite 4 months adjusted age.​ The neurologic co-morbidities (likely absent corpus callosum) suggest at least part of the etiology for the abnormal swallowing and likely; altered oral-pharyngeal reflexes that underpin feeding. There may be other components of his history that might further inform a differential to guide a plan of care. I would suspect there might have been a VFSS early on in the NICU unless he was so neurologically devastated that the team determined a VFSS would not change his management and proceeded with a G-Tube/Nissen; or if he did not swallow his saliva, we would likely not do a VFSS.

To start problem-solving, it will be helpful to understand what you see clinically, especially related to postural and oral-pharyngeal tone, oral-pharyngeal reflexes, interest in own hands to face/ mouth, need for suctioning and response to suctioning, any spontaneous swallows observed, any ENT consult results.

Very challenging patient with multiple complex issues that are likely to be enduring and progress likely to be slow.

I hope this is helpful.

Pursuing Certification in Lactation

My colleague Mary Lou Sorey, MS/CCC-SLP, IBCLC is a guest columnist. She has provided services in pediatrics and specifically in the NICU for many years at University of Mississippi Medical Center. Her post provides some very helpful answers to a frequently posed question: “What is the best way to pursue certification in the field of lactation in lactation?” Her thoughtful comments follow.

As a certified SLP and IBCLC (International Board-Certified Lactation Consultant) now practicing in a Level IV NICU, I have often been asked by my colleagues about pursuing certification in the field of lactation. Most want to know how to go about obtaining this additional certification, as well as if I have found it to be beneficial in my practice.

I have found the certification to be helpful, and the education most fascinating! I have used this education/certification in various ways over the years. On occasion, I have been allowed to initiate first feedings with preemie babies at the breast when MD allows, and hopefully this will become more prevalent in our unit with ongoing education regarding the benefits of this practice. We have lactation consultants in our hospital that follow the moms who deliver here, so I am typically not directly involved with those moms. I do, however, ask all of my patient’s moms who are providing EBM for their babies about pumping, make suggestions for increasing milk supply, and troubleshoot problems that may warrant further referral to our lactation consultants. This has been especially helpful for the moms who didn’t deliver at our hospital and don’t have one of our lactation consultants following them. 

There are several different lactation certifications that one can pursue, i.e. Certified Lactation Educator (CLE), Certified Lactation Consultant (CLC), Certified Breastfeeding Counselor (CBC), or International Board-Certified Lactation Consultant (IBCLC), each with its own set of educational and/or clinical requirements.

The one I am most familiar with is the IBCLC offered through the IBLCE (International Board of Lactation Consultant Examiners). The IBLCE offers three different certification pathways from which to choose but requires all candidates to complete 14 health science courses (either as an IBLCE Recognized Health Care Professional OR complete coursework in each subject) and 90 hours of lactation education. The IBCLC exam is required for certification, which is maintained by submitting continuing education hours (called CERPS) after the first 5 years, and by retaking the board exam every 10 years from date of certification. Specific information for each pathway can be found at https://iblce.org.

Here are some excellent resources for obtaining more information and education for those who are interested in pursuing certification in the various areas of lactation.

Problem-Solving: Fluoro Time for Neonates

Question:

At the hospitals that I work at we have outdated machines that only capture video swallow studies at 6 frames per second. Are the restrictions the same for fluoro time (I think it’s about 2 min recommended fluoro time at 30 frames per second for peds and neos)?

Catherine’s Answer:

The low frame rate will of course limit the objectification of swallowing physiology, unfortunately, and sometimes can lead to the need for increased exposure time. Multiple citations by Heather Bonilha Shaw would be helpful as you advocate, along with your radiologists, for equipment that provides 30 fps.  Given your situation, ALARA (as low as reasonably achievable) should remain your guide. That said, as I teach across the US and survey attends at my swallow study seminars, is most typical that with neonates, the aim is the least amount necessary but less than 2 minutes; with pediatric patients, less than 5 minutes. Of course, co-morbidities, compliance, previous exposure to x-ray/radiation, and clinical impressions about physiology as your go along in the study, all must be considered.

Our tech tracks the exposure time as we go along, the rad and I are very aware, and at each juncture I am asking myself “have I objectified physiology sufficiently? Do I need more time?” and if so I am very thoughtful about continuing or not. if I need a few more swallows to better elucidate physiology or complete a differential, or to objectify the likely positive impact of an intervention, I usually discuss it with the rad and we agree on further time based on a determined required need. Most infant studies are less than 2 minutes exposure and most of our pediatric patients less than 3 minutes, at 30 fps.

At the end of each study, I think always ask myself, ” is there anything I could have done differently to reduce exposure time?” Maybe not but it keeps my always trying to do better for my little patients. Heather is on the ASHA list serve, and, I am sure, can add her always appreciated thoughts. Her recent commentary (see list serve archives) on a paper suggesting 15 fps in pediatrics so eloquently explained issues even in 15 fps for our population that may also be useful in helping to make the case for equipment that provides 30 fps.

Problem-Solving: Respiratory rates in neonates

Question:
Hot topic and in need of evidence based research regarding bottle feeding the premature infant (or term infant) with tachypnea.

What is everyone’s practice?  No PO feeding if respiratory rate above 60? 70?  Would appreciate research articles and your hospitals guidelines!

Catherine’s answer:

To my knowledge, there is no research to guide practice but rather the it is often neonatologist training,  preference and the extent to which intake is a key driver in a particular NICU. Neina Ferguson published an informative paper in 2015 about preterm infants in  the NICU that correlated tachypnea during PO with subsequent aspiration in radiology.

Ferguson, N. F., Estis, J., Evans, K., Dagenais, P. A., & VanHangehan, J. (2015). A retrospective examination of prandial aspiration in preterm infants. Perspectives on Swallowing and Swallowing Disorders (Dysphagia), 24(4), 162-174.

The paper did not look at impact on physiology in detail, but I clinically see in the NICU population that tachypnea can alter physiology without witnessed aspiration or penetration under fluoroscopy, and thereby create risk for airway invasion.

Some neos write orders to PO if infant is “comfortably tachypneic”, RR under 70.  “Comfortably tachypneic” is a almost parodical , in that tachypnea is rarely co-occurring with a comfortable looking infant, rather infants who are tachypneic may often be  exhibiting other signs of physiologic stress (e.g., nasal flaring/blanching, suprasternal and/or supraclavicular retractions, chin tugging). Increasing RR leads to more shallow insufficient respirations. The need to breathe often and rapidly will create challenges in the swallow-breathe interface, and cause breathing and swallowing to uncouple. It takes a second to complete the pharyngeal swallow, so then a RR over 60 clearly increases risk for airway invasion.

Respiratory Rate, my RT mentors tell me, doesn’t exist in isolation but is rather a part of a bigger picture. Much like, they say, level of respiratory support required does not exist in isolation. It’s each infant’s bigger picture that guides us.

As we advocate and make determinations of relative risk with PO feeding for our preterm infants, we really must look at each infant in the setting of his unique history and co-morbidities and their unique attendant sequelae. An infant post HIE just weaned or HHFNC will require a different algorithm than the former 24 weeker with CLD, contrasted with the term infant who is s/p TEF/EA repair. And, as Dr Coyle says, that is ok. One algorithm won’t work for every patient and it shouldn’t. All of my examples are infant who often have risks for airway invasion but the nuances of each infant will likely yield a slightly different profile from which to problem-solve, with the team.

That is the challenge of our work in the NICU. To look at each infant as a unique patient, and,  in the setting of what we know about him, and what we see clinically, make a well-thought out educated plan to minimize risk, articulate those risks as best we can to the team, establish interventions that optimize safety and assess their impact on an ongoing basis.

In the NICU , we are required to  live in the grey zone…no easy questions and there are no easy answers, more questions than answers, constantly thinking and re-thinking.  Just keep “listening” to each infant Tara, like you are doing, and especially partner with RTs and a neonatologist that respects the complexity of feeding and swallowing so they can think along with you.

Problem-Solving: Vocal Cord Paralysis and Sidelying

Question:

Does anyone know of any research articles regarding the effectiveness of putting an infant with a left vocal fold paralysis in a sidelying position for bottle feeds? Also, what are your thoughts about performing an MBS or FEES prior to initiation of PO feeds?

Answer:

To my knowledge there are no randomized controlled trials or research studies regarding this intervention. The pediatric ENTs who took me under their wing early on in my career suggested it and theoretically it made sense to me. While its proposed purpose (i.ie, placing infant with a left vocal cord paralysis R side down for PO feeing) is to utilize gravity to assist by passively bringing the paralyzed cord to midline, it is unlikely that can simulate true effective closure as one would observe in the setting of normal vocal cord motility.

In addition, if there are other co-occurring co-morbidities that adversely affect airway, postural or swallowing function, those most also be considered in the differential. However, combined with other interventions such as controlling flow rate, co-regulated pacing and resting, we have consistently seen improved dynamic swallowing objectified under fluoroscopy in radiology. That clinical wisdom is a level of evidence base that has helped to guide my practice.

There is also a high risk for a paralyzed R vocal cord post ECMO, so many of our cardiac infants and select preterms who require ECMO. Similarly, I have both clinically and instrumentally observed a left side down position in the setting of a R vocal cord paralysis to be a useful intervention to trial.

Once again, need to consider all co-morbidities that maybe relevant to guide us. I prefer that infants not have their first PO feeding experience in radiology. It doesn’t allow me to complete a cautious limited clinical examination of PO feeding prior to the instrumental, during which time I can begin to formulate a differential regarding the full picture (i.e., potential effects of respiration, state, and other co-morbidities on the infant’s feeding/swallowing function in the context of the infant’s history. Also, during that first feeding, when sensory-motor maps are being established and recruited, they must be on the x-ray table or in an infant seat. That said, we recognize that high risk for airway invasion in the setting of both L and/or R vocal cord motility issues. If clinically indicated, I prefer at least 1-2 very small brief PO feeding experiences with me while I trial the interventions and allow the infant to experience sensory-motor learning under optimal conditions. This can be as little as 5 mls. Because we recognize that swallowing physiology needs to be objectified to guide management for such an infant, an instrumental assessment would then follow. FEES would clearly inform our differential, and a VFSS would provide insight into the dynamic swallow pathway. I hope this is helpful.

Problem-Solving: Sensory Normalization with Rubinstein-Taybi Syndrome

Question:

I recently started treating a 2-year-old little girl with Rubinstein-Taybi syndrome in outpatient feeding therapy. She has had a G-tube since she was 1 month old and has barely eaten PO. I am just trying to get her to take PO to get her to a VFSS, as the last VFSS she had, she aspirated after the swallow due to residuals in pyriforms. No cough response at the time. She is literally so averse to even a dry spoon touching her lips, she tightens her lips and turns her head no matter how many times I do it in an attempt to desensitize her. The one time I touched a dipped spoon to her lips, she had a moderate-severe gag response. And the amount of vanilla pudding in the bowl of the spoon was so minimal, I couldn’t really lessen it….we just went back to a dry spoon. I’ve tried the Honey Bear straw, I’ve tried a spoon with cold water, Dum Dum lollipops….no luck. I’m really at a loss. We’ve had 4 sessions so far and no progress…and even possibly a regression, as she now won’t even sit in the high chair for more than 10 minutes without getting restless, reaching out, wanting to play and/or sit on parents laps. She has no verbal communication, only whining and reaching arms out. She can identify some things but it’s inconsistent. However, I know her receptive language and memory are her strengths. Any suggestions/feedback/advice is greatly appreciated! I need all the help I can get with this little one.

Answer:

Normalizing her sensory-motor/postural system (through partnering with a sensory integration trained OT) and normalizing her oral-sensory system will be a critical first step. PO feeding skills are built on a well integrated sensory system, often a key area of need for children with this diagnosis.

A swallow study likely isn’t a next step for her until she is accepting well graded positive oral sensory input. There is likely some level of swallowing impairment that won’t be fully understood until the sensory system is normalized, which will allow her to then begin to accept trace tastes of purée to eventually support an instrumental assessment of swallowing physiology.

Her progress will be slow due to her underlying diagnosis and a sensory system that has been impaired since birth. These systems are complex, require heavy neuro underpinning and require new sensory- motor maps be created in the brain through child-guided well graded sensory motor learning. Co therapy with an OT focused on sensory treatment with SI intervention would be a great facilitator. Parents can learn along with you about the need to think of small steps “toward” eventual PO but that is not the immediate goal due to the many little steps of learning required before she is truly ready to eat/drink orally.

Problem-Solving: Former Preterm with Beckwith Wiedemann Syndrome

Question:

I have a 34 week premature infant with Atrial flutter and Atrial septal defect that I just started seeing who has Beckwith Wiedeman Syndrome. The pediatrician recommended solid food feedings due to not taking his formula consistently. Mom only gives him baby food at night and he eats about half a container but seems to enjoy it. He had a MBS since he was receiving thickened formula with oatmeal on 6/5/19. He was clear for thin liquids via Avent level 1. He got frustrated with nipple so SLP in outpatient ok’d him to use Avent level 2. According to his MBS, he had oral transport/lingual motion impairment and oral residue. His swallow response is impaired at level of pyriforms, laryngeal elevation and anterior hyoid excursion are also impaired. At rest, child’s tongue protrudes and when he sucks on the bottle and when spoon feedings are tried, he has a tongue thrust. Coughing is noted during bottle and spoon feedings and when the bottle is pulled out of his mouth every 2-3 sips to help him breathe, he seems to have difficulty latching onto the bottle. I’ve tried palpating gently under his chin and noticed his tongue recessed into his mouth for a brief time, and have tried a ‘j scoop’ with the spoon when fed him. I just wonder what other treatments you would recommend I try since his doctor wants to try therapy before surgical treatment of macroglossia.

Answer:

Sounds like he is a former 34 weeker who you are following in the community. What is his adjusted age now?

Being a former preemie, as opposed to a former full term infant, adds some other challenges to his BWS that might be playing a role, such a respiratory co-morbidities. Sounds as though he was sent home from the NICU as a full oral feeder, but quality may not have been part of the assessment for readiness to be a full PO feeder, rather volume was.

What looks like tongue thrust may actually be the tongue moving forward with onset of motion, due to the lack of space in the oral cavity for his enlarged tongue as it moves posteriorly and an adaptive response on the part of the infant to maintain his upper airway.

Sounds like he was sent home without any respiratory support to assist with airway maintenance. Many infants with BWS require trachs to assure a consistent patent upper airway. Even so, some who manage to be discharged without airway support can readily destabilize a fragile upper airway with the act of swallowing during feeding. The need for the base of tongue to retract, and the large thickened blade to move posteriorly as part of the swallow, can actually “create” a sense of further airway obstruction with the act of swallowing. In addition, the thickened blade with intrinsic tongue muscles that lack thinning and cupping can create challenges with bolus control orally.

The macroglossia also can alter mandibular alignment, leading to subluxation. It also inhibits a closed mouth posture, which can work against establishing the necessary anterior seal on the bolus to help drive the swallow.

Often behaviors during feeding may be related to the struggle during feeding to manage the bolus and maintain the upper airway, and can lead to adaptive behaviors, which then create maladaptive feeding behaviors and long-term struggles with eating/drinking.

Sounds like with Avent 1 flow in radiology there was a delay in swallow initiation with premature entry to the pyriforms. It is likely the bolus is poorly managed due to the adverse effects of BWS noted above, so it would be important to objectify the effect of the change/increase in flow rate with Avent 2 on his swallowing physiology, as his physiology sounds precarious. The coughing with spoon and bottle suggest fluid has approached or entered his airway.

Even if he there was no witnessed aspiration or laryngeal penetration during the VFSS (which is a moment in time), he is at high risk for airway invasion and onset of aversions due to the struggle to feed. Most events of aspiration are silent in the infant population,  and he is also giving us some signs, so he is likely more worrisome.

I think the doctor’s well-intentioned goal of wanting him to PO feed before surgery may have been made without his understanding of the impact of BWS on swallowing physiology and the swallow-breathe interface, and may be counter productive and perhaps not safe for this former preemie. Muscular and structural restrictions such as those with BWS often require us to take a step back and look at the co-morbidities and their overriding influence on swallowing physiology not just on intake, which is at times challenging for our medical colleagues.

Problem-Solving: Late Preterm with Sequelae from Mandibular Hypoplasia

Question:

I am presently working with an 8 month old who is s/p cleft palate repair, x 1 month. She is an ex 35 weeker with a trach and PEG tube. Her list of problems/diagnoses: Pierre Robin Sequence, Peter’s anomaly, ASD, Stankiewitcz-Isidor Syndrome, retrognathia, and micrognathia. Currently, she eagerly accepts the pacifier and bottle. We are using Dr. Brown’s level 1 with the valve but this flow seems a little fast and are trying the Newborn level. However, her tongue pulls back and therefore is not wrapping around the nipple for traction. She gets approximately 10-15ml in 30 min only due to compression. Any time that I attempt to put a gloved finger on top of her tongue to work on drawing it forward she gags. At best she reluctantly allows my gloved finger with formula just to the tip of her tongue. Any recs? Also, what resources/books do you recommend for infants/children with cleft palate?

Answer:

I think right now the cleft is the last important factor and is likely not contributing to what you are seeing with PO attempts. Her complex co-morbidities make a her a fragile feeder,  I would think, with high risk of silent airway invasion. The muscular and structural restrictions to the mandible, and therefore, to the tongue (glossoptosis) associated with the Pierre Robin and Peter’s Anomaly, likely lead to adaptive behaviors in an attempt to protect the airway. That then leads to the maladaptive behaviors you are seeing. My guess is her trach was placed  to establish an airway (not for long-term ventilation), so without a PMV (which she cannot wear due her airway obstruction), she also has no taste, no smell and has no subglottic pressure for airway protection. I would not PO with what I know, but rather, work on readiness non-nutritively right now. ENT would be very helpful  to guide your plan of care by assessing growth and readiness for decannulation in the future.