Problem-Solving: RR and PO Feeding in the NICU

QUESTION: I have a 33wker with a VSD that nursing is PO feeding every feeding. Are there studies regarding respiratory rate while feeding? The infant looked comfortable at 65 and below but I told nursing to stop feeding with rate above 80 (or allow major rest break for her to slow it down because she’s often cueing).  I’d love hard data to support those numbers


I don’t know of any randomized controlled trials that yielded this data. Clinically we know that spontaneous RR is typically different than monitored RR, due to an artifact created by the monitor not consistently sensing rapid shallow breaths. We gather he best data by counting the spontaneous breaths, as it’s more reliable. Anytime the RR is above 60 we know there is greater risk, as it takes a second to complete the pharyngeal swallow. RR over 60 increases risk that the swallow and breathing will co-occur or “collide” as I like to say to parents. Work of breathing often goes hand in hand with the RR but can often be a more worrisome indicator of risk for airway invasion. As the effort goes up, breaths are more shallow, there is then less tidal volume, and the infant is more likely to need an urgent breath. In those moments, the need to breathe will override the swallow. Often this means opening the airway too early or not fully closing it at the moment of the swallow. Because NICU infants are at higher risk to silently aspirate, the infant described may show no outward signs. We know he is a 33 weeker – which means to me that he was born at 33 weeks. What is his PMA? Or are you meaning he is now 33 weeks PMA; if so, what was his GA? Helps me make sense of his risk. The VSD will drive up WOB and RR at baseline, and with the aerobic demands of feeding. Does he have an otherwise unremarkable history except for VSD? Currently requiring respiratory support? What are saturations like with PO? What physiologic and behavioral stress signs do you see even with interventions? What interventions are the nurses using to protect him? Perhaps having you offer guided participation while a nurse feeds and you think along with her, might build a conversation about airway protection and neuroprotection, both of which are likely at risk given what we know.

Problem-Solving: Thickening Post VFSS


I work in a pediatric hospital, and we’ve been running into difficulty when it comes to the recommendation to thicken liquids. Our speech dept procedure is not to recommend or endorse a specific product and place that responsibility on the physicians after we relay the MBS results. Often GI doctors are more comfortable with thickening choices, contra-indications, etc. but our pulmonologists and cardiologist feel that they do not have the training to make those choices and don’t feel comfortable. As a dept we want to support our doctors and I was hoping another facility has run into this issue or addressed it and could share their processes. Thank you!


It is important I think to discuss options with families and providers, and consider home environment, access, cultural preference, caregiver capability and potentially the providers don’t have that insight. This goes a long way towards recommendations and strategies that are more likely to be carried out by families. Along the way we help providers who are not GI specialists benefit from our problem-solving and our ability to bring the current evidence-base to the conversation.

I rarely thicken liquids these days. When it is indicated as a last-resort intervention, based on objective data regarding pathophysiology and potential airway invasion observed during the VFSS in the setting of that child’s co-morbidities, I find a few things quite helpful.

During the VFSS, we have likely utilized particular thickeners that give us objective data about their impact, have flow tested the liquids with those thickeners, and have some impression as to what may be optimal (risk-benefit ratio from swallowing perspective). We might then offer that data as a part of the problem-solving discussion with the physician/team, recognizing that the prescriptive nature of what is ultimately determined by the physician’s order will be a biproduct of further discussion. This is an opportunity to collaborate about patient care and builds relationships with the medical team. This bringing together of each professional’s data and perspective has been referred to as “cross-fertilization”. I love that term and its implications for how we practice or might optimally practice as lifelong learners. With cross-fertilization, everyone’s engagement exposes all professionals to different bodies of scientific literature knowledge, as that supports collaborative practice. We all benefit from these exchanges, especially our patients and families.

Another resource to share with physicians that is, to my knowledge, part of the latest evidence-base we have available, is this wonderful paper by the team at Boston Childrens, including Kara Larson SLP and two amazing GI docs. As it states, the purpose of this review is to discuss current knowledge and recent findings regarding clinical aspects of thickeners for pediatric gastroesophageal reflux and oropharyngeal dysphagia. We review evidence for thickener efficacy, discuss types of thickeners, practical considerations when using various thickeners, and risks and benefits of thickener use in pediatrics.  

Duncan, D. R., Larson, K., & Rosen, R. L. (2019). Clinical aspects of thickeners for pediatric gastroesophageal reflux and oropharyngeal dysphagia. Current Gastroenterology Reports21(7), 1-9.

Problem-Solving: Young Infant with Mandibular Hypoplasia and Glossoptosis


I have an infant (2-week-old) coming in for a feeding eval next week (mother reported difficulty latching on breast and bottle, feeds last 30-40 min, infant not gaining back birth weight), referred by ENT, script says micrognathia and glossoptosis. I did a quick research scan and didn’t find a lot regarding micrognathia besides osteogenesis. Open to suggestions or any research articles you can point me to regarding this topic… who to refer to? any other treatment you’d recommend?


This clinical presentation in infants can be quite complex. Sucking, swallowing and the swallow-breathe interface can all be affected, as can overall postural control and sensory-motor learning. Once you see the infant, can begin your differential about what relevant areas are impacting swallow function, and what other consults or diagnostics might be helpful.

Good that you already have an ENT involved who has evaluated the infant and provided impressions. Do you know if there was a flexible scope done as part of the ENT consult? You may want to check, as that will also be helpful to better understand the functional dynamics of the base of tongue on this infant’s swallow. Due to the glossoptosis, you will likely hear inspiratory stridor created by intermittent obstruction of the base of the tongue against the posterior pharyngeal wall. This can interfere with swallow-breathe interface and alter swallowing physiology. An elevated swaddled sidelying position will help to utilize the effects of gravity to help bring the mandible forward. An instrumental assessment of swallowing physiology will likely be a part of your differential, as there is often altered oral and pharyngeal phase physiology that creates risk for both silent and symptomatic airway invasion with this clinical presentation.

It is also likely that there may be associated tethered oral tissues, as the timing of developmental emergence of structures in utero predisposes these correlations. As mentioned already, the tethering, if it is present, can actually help the infant to compensate for the glossoptotic forces and therefore help keep the tongue from falling farther into the hypopharynx.  This reminds us of how important it is to not “signal react” to one aberration (e.g., tongue tie) , without considering its dynamic influence on the big picture, i.e., releasing the tethering would cause more problems, given this infant’s co-morbidities. So, compensating for the adverse impact of possible tethering on the suck may be a focus. The infant may have a “compression-only” sucking pattern r/t the glossoptosis in and of itself, as it often leads to a thickened and bunched lingual body (intrinsic and extrinsic tongue muscles often don’t develop properly in the setting of this malformation). The altered lingual control can affect not only establishment of suction but also oral bolus control, and cause “problems down the line” (i.e., with pharyngeal function). The Dr. Brown’s nipple with specialty valve may work but sometimes the tongue may be too far back in the mouth to even permit an effective latch with that system. An option would be the Haberman, but without any squeezing of the teat; increasing flow rate would be contraindicated with this clinical presentation, as it would increase bolus size and adversely affect bolus control and airway protection

Co-regulated pacing and resting will be essential, as the infant’s WOB (work of breathing) will be increased. Breathing is typically adversely affected by challenges with airway maintenance created by the need for further retraction of the tongue base that is part of the swallow process. For this infant, that will make it difficult for the infant to maintain the airway as it reconfigures from a respiratory tract to an alimentary retract dynamically during feeding.

Mother will likely need your support to focus on infant-guided feeding (versus volume), learning about what the infant’s behaviors during feeding mean (what infant is trying to communicate), waiting for the infant to root (that suggests he is then, at that moment, better managing his airway and is ready to suck), and thoughtfully and contingently offering interventions to optimize safety.

This wonderful paper by my friend and colleague Laura Brooks at Children’s Healthcare of Atlanta provides valued additional insights for my rationale to consider a swallow study to objectify physiology, given this infant’s co-morbidities:

Brooks, L., Evans, S., Alfonso, K. et al. The Role of Dysphagia Assessment in the Identification of Upper Airway Obstruction in Infants. Dysphagia (2022).

This pathophysiology Laura describes is not uncommon when an infant presents with these challenges. The alterations along the swallow pathway created by glossoptosis may be part of the reason for poor intake. Perhaps the infant is trying to protect his airway when he purposefully disengages during feeding. I appreciate Laura’s adding to our evidence base and reinforcing that “co-morbidities matter,” as I always like to say.

Problem-Solving: NICU infant aspiration versus LPR/EER?


I have a question about an NICU patient who is currently 39-3, formerly 25-2. BPD, chronic respiratory, very prolonged intubation. I did pre-feeding milk drops, etc but she never even began cueing until 35 weeks when on 2Liters. I used a Dr. Brown’s Ultra Preemie and progressed PO very slowly due to increased WOB. She has now had steroids and was just weaned to room air this past week. She takes full volume and is doing much better pacing herself and I have upgraded her to a Dr. Brown’s Preemie.  She has always had spells and apnea but for the past 3 weeks every time you go to burp her, she bears down like she is trying to maybe protect her airway from reflux, she then holds her breath and desats. I have tried smaller volumes and burping more frequently but no luck getting her burp until further into the feeding. The desats are not as low as they once were but I just feel like I see so many babies that are suffering from large volumes and experience reflux. She does have occasional choking spells and I offered to do MBSS but was shot down. The neo that day wanted to thicken with rice. We haven’t been thickening very much since I came to the unit and when the neos want to thicken they choose oatmeal. There is also a SIM spit up formula for term babies that is thicker. What should I do in this situation? I fear I am missing aspiration but most of the babies I take for fluoro don’t aspirate and I just see the retrograde flow (reflux). I have read laying them on their right side may help. What are our research proven reflux tools – I know a lot of the answer is -time to mature but is there anything else I should be doing?



Sounds like you have offered her thoughtful preparation for infant-guided, neuroprotective feeding. I’d be extra careful about letting her set her own pace, given her respiratory hx. Even healthy term NBs don’t “pace themselves” until closer to 2 months of age per the research. Though she may take breaths on her own with PO, given her hx it is likely the breaths may be even a bit latent or a bit insufficient, or she may have some element of gulping that results in air ingestion. Have you tried burping in elongated sidelying? I find that better takes the pressure off the abdomen than semi-upright burping in caregiver’s lap (since increased abdominal pressure which can provoke EER/LPR). The choking could be co-occurring EER/LPR or events of airway invasion/t mistiming of swallow-breathe interface, which is what we typically see if we were to do a VFSS on an infant with her hx and diagnoses. We rarely thicken too. Seems with Dr Brown’s nipples and contingent co-regulated pacing with resting and elevated elongated sidelying we can minimize EER/LPR events as much as possible and avert need to thicken for reflux. At the same time, we are optimizing the swallow-breathe interface with the same interventions that also minimize/inhibit gulping (and air swallowing). Sim Spit up has a slightly increased viscosity which may help – but I’d try the more strict/frequent pacing. Yes, our neos are strict about VFSS understandably but this hx is worrisome and is the classic presentation that is a silent aspirator when objectified.  Studies show that L side down the for first hour post feeding then R side down the second hour post feeding is optimal based on gut anatomy –but RNs must balance head shaping and “changing position with cares” as well, so it cannot be a perfect world. This is a fabulous paper on reflux! Does not include newer meds due to publication date but is otherwise so wonderful!— Schurr, P., & Findlater, C. K. (2012). Neonatal mythbusters: evaluating the evidence for and against pharmacologic and nonpharmacologic management of gastroesophageal reflux. Neonatal Network31(4), 229-241.


Problem-Solving: 2 -year-old with Pierre Robin Syndrome

Question: I have a complex case I have been following since her time at our NICU. She is 2 years old, and I just completed a repeat VFSS (outpatient, her seventh to date) which continues to show significant dysphagia with high aspiration and airway obstruction risk.

History is significant for Pierre Robin sequence (chromosome deletions at 10q11 and 20p12) and cleft palate. She was born full term but required intubation after birth for critical airway. She required mandibular distraction hardware placement for about 2 months, has required supplemental nutrition by means of a feeding tube since birth (has had a PEG for over a year), and had a bilateral palatoplasty around 18 months of age. She’s been followed by feeding therapy, but despite recommendations for NPO because of her significant risks, she really wants to eat and drink. She pulls food off of the table from her siblings’ plates and has been eating/drinking regular/thin without specific correlation to any respiratory compromise.

I wish I could insert a fluoro clip here as I think it will be hard to spell this out… her swallow is significantly uncoordinated. With all consistencies the bolus reaches the pyriforms and at the onset of her “swallow” she presents with immediate regurgitation to the oral cavity and nasopharynx. No barium enters the esophagus with the initial swallow, it almost appears that the timing of UES relaxation follows tongue base retraction after the majority of contents have been redirected from the hypopharynx. This sequence is repeated 18 times prior to what appears to be a complete swallow, during which the contents that weren’t incidentally passed through the UES are cleared through the pharynx. Laryngeal penetration and aspiration at the height of the swallow occur during most of the uncoordinated “swallows” (which is silent). The pattern is the same with all consistencies and is paired with an open mouth posture. When provided with tactile cueing to keep her lips closed, she appears to have the coordination/pressures needed to clear small boluses with single swallows, but her adaptations seem to drive the motor planning train at this point. I ethically could not proceed with solid foods even though mom called two months ago to ask if we could ‘try solids no matter what’ during the study… they had hot dogs for dinner last night and brought pieces of hot dog to the study today. I have no explanation for how a choking event did not happen.

My heart really goes out to this family; they need a lot of guidance, and it has been a journey for them. Our oral maxillofacial surgeon and gastroenterologist have agreed to have a sit-down care conference with the family which I am extremely grateful for… my question is in regard to where to go from here. I think she needs intensive feeding therapy at this point and the clinics that I am most familiar with in our area are behaviorally driven to help kids wean from tube feedings… but she is a special case in which she really wants to eat and drink but is not safe to do so… does anyone have any specific cleft palate clinics that they have worked with? Mom is very open to this and was very open to me posting the patient’s case here to get some ideas for them.

Superior based pharyngeal flap surgery is in the discussion, but until her adaptive “swallows” are not the driving force of her function, I don’t see how she will safely manage as I think her ability to redirect boluses into her nasopharynx are her saving grace (as strange as that sounds).

Any and all help/insight is appreciated.


Answer: The infants and children we see never cease to amaze me with their adaptive behavior to accomplish a task in the face of such challenges. Bonnie Martin Harris always reinforces the dynamic nature of the swallow pathway, and how alterations in one point along that pathway can create compensatory behaviors along the pathway that may not always be beneficial but may indeed be maladaptive behaviors. What is the source of the alteration versus the compensatory behavior always needs to be sorted out, and you have done that so very well!

I have had three children with similar clinical and videofluoroscopic presentations. They each had mandibular hypoplasia, only one had the benefit of mandibular distraction. The impact of mandibular hypoplasia on motor learning in utero is not always fully appreciated. Early on, it creates muscular and structural restrictions to base of tongue integrity (decreased ROM, decreased posterior prolusion, decreased BOT retraction for the dynamic swallow). The fetus swallows amniotic fluid from 17 weeks on, and so by birth at term, has had 23 weeks of motor learning to help build the motor maps that underpin the swallow. Mandibular hypoplasia leads to reduced oral cavity space, this displaces the tongue body, leads to an altered tongue position, typically retracted back into the oral cavity and often with some form of glossoptosis; it also can create muscle shortening that will impede full ROM for the necessary base of tongue retraction. Even post MDO (Mandibular Distraction Osteogenesis), many infants continue to show reduced BOT retraction on VFSS for this reason. That’s why MDO is not a “fix all” for Pierre Robin sequence or mandibular hypoplasia, with its attendant alterations in muscular function, though MDO is unfortunately viewed as such by some medical professionals (i.e., “the infant was distracted, why doesn’t he eat?”). The co-occurring open mouth posture likely adversely affects an anterior seal on the bolus, which, along with reduced BOT retraction, acts as another impediment to generating the pressure required to relax and open the UES. The resistance to bolus flow causes the bolus to take the path of least resistance. The need to establish the more typical motor plan in order to habilitate (or maybe even rehabilitate at this point despite her young age) feeding skills is important.

Working on an anterior seal (lots of fun ways to do that at her age) and pressure generation with smaller boluses would be helpful. I wonder if a short repeat study to objectify optimal viscosity/viscosities for pressure generation might be informative, and like a short biofeedback for her, if she is cognitively appropriate, and perhaps to objectify the impact of optimal cueing strategies, utensils and neuromotor facilitation provided. Pharyngeal manometry to better objectify the role of pharyngeal pressure generation in bolus flow.

I so appreciate your critical thinking and living in the gray zone as I like to call it; where you are ok with pausing to think of possibilities, weighing them and asking more questions, instead of rushing to an answer. I’d be happy to work alongside each of you anytime.

Research: Down Syndrome and Swallowing Pathophysiology

I wanted to share a summation of recent research on prevalence of pathophysiology in infants with Down Syndrome that adds to our evidence-base. It suggests that a high index of suspicion is warranted, and watchful vigilance is required.

Narawane et al (2020) found high prevalence of both oral and pharyngeal dysphagia (89.8% and 72.4% respectively) in infants with Down Syndrome during VFSS. Laryngeal penetration was present in 52% and aspiration in 31.5%, often with thin liquids. When aspiration occurred, it was “silent” in 67.5%.

Jackson et al. (2019) looked at presence of deep laryngeal penetration and/or aspiration (on VFSS or FEES) in infants with Down Syndrome younger than 6 months versus those 6-12 months old. 31.9% of the younger group showed abnormal findings, compared to 51.3% in the older group. CHD and laryngomalacia were identified as risk factors for aspiration.

Stanley et al (2019) looked at 100 infants with Down Syndrome younger than six months via VFSS. 96% showed abnormal results. CHD was not a risk factor in this study, but co-occurring risk factors were desaturation during feeding, airway/respiratory anomalies, being underweight and prematurity.

Jackson et al. (2016) looked at older children with Down Syndrome (mean age of 2.1 years), and found oral motor difficulties in 63.8%, pharyngeal dysphagia in 56.3% and aspiration in 44.2%. Aspiration events were mostly “silent”.



Narawane, A., Eng, J., Rappazzo, C., Sfeir, J., King, K., Musso, M. F., & Ongkasuwan, J. (2020). Airway protection & patterns of dysphagia in infants with down syndrome: Videofluoroscopic swallow study findings & correlations. International journal of pediatric otorhinolaryngology132, 109908.

Jackson, A., Maybee, J., Wolter‐Warmerdam, K., DeBoer, E., & Hickey, F. (2019). Associations between age, respiratory comorbidities, and dysphagia in infants with down syndrome. Pediatric pulmonology54(11), 1853-1859.

Jackson, A., Maybee, J., Moran, M. K., Wolter-Warmerdam, K., & Hickey, F. (2016). Clinical characteristics of dysphagia in children with Down syndrome. Dysphagia31(5), 663-671.

Stanley, M. A., Shepherd, N., Duvall, N., Jenkinson, S. B., Jalou, H. E., Givan, D. C., … & Roper, R. J. (2019). Clinical identification of feeding and swallowing disorders in 0–6 month old infants with Down syndrome. American Journal of Medical Genetics Part A179(2), 177-182.


Significance of Laryngeal Penetration in Pediatrics: Research and Reflection

In the neonatal and pediatric population, evidence is still emerging to guide our processes during the instrumental assessment, interpretation and analysis of pathophysiology and subsequent recommendations. Our time in radiology is such a small window, often with limited, and at times tenuous, data. We then need to consider that data in the setting of that infant’s/child’s unique co-morbidities and history, which then give meaning to the data we have collected.

There is no cookbook for pediatric swallow studies; cookbooks were made for cooking, not for instrumental assessments. Knowing potential interventions, but also what interventions would be contraindicated based on pathophysiology/history/co-morbidities is the starting point. What we then recommend may indeed tip that balance between risk-benefit, and in either direction. Optimizing the risk-benefit ratio for the infant/child requires us to utilize critical reflective thinking, with a focus on the nature of the pathophysiology, the biomechanical alteration/impairment, and its implications for that unique infant/child. In drilling down to that infant’s/child’s “story”, we then realize that a plan for baby A with the same objective data from radiology may not be appropriate for baby B.

The nature of the pathophysiology in the neonatal/pediatric population has nuances that reflect the dynamic interaction of the developmental trajectory of motor learning with evolution of the swallow. Superimposed on this, then, are the co-morbidities that increase risk, especially prematurity, CLD, CHD and other diagnoses that adversely affect cardio-respiratory integrity.

The evidence-base in the literature to guide us is emerging and is still in its infancy. Laryngeal Penetration (LP) has been associated with negative clinical outcomes in subsets of the pediatric population, including increased risk for PNA and aspiration (Gurberg et al, 2015). Duncan et al (2020) out of Boston Children s Hospital found in their study that laryngeal penetration is not transient in children < 2 years of age and may be indicative of aspiration risk. In their study, on repeat VFSS: 26% with prior LP had frank aspiration. The authors remarked that “Any finding of LP in a symptomatic child should be considered clinically significant and a change in management should be considered”. That may be a change in position, change in nipple, change in cup, adding a control valve, limiting bolus size, pacing, slow rate of intake, smaller sips, not necessarily thickening.

In such a scenario, thickening is not a solution but may be an interim step along the way to allow time for motor learning by the infant/child and for us to address the underlying pathophysiology. Thickening is not without its own attendant sequalae and is always our last resort in pediatrics. Brooks (2021) looked at potential options for thickening that may be less problematic for and better tolerated by our pediatric population, which can include certain purees, such as fruit or vegetable purees and yogurts.

Duncan et al in 2019 stated that thickened liquids are indicated “When symptoms pose greater risk than negative effects of thickeners”. In their study, intervening when penetrations were observed yielded symptom improvement, and reduced hospitalizations, especially pulmonary–related. Greatest improvement was observed with thickening (91%). Benefits of thickening when indicated via critical thinking can include swallowing safety, increased intake and parent satisfaction (Coon et al, 2016; Duncan et al, 2019, Krummrich et al 2017)

In addition, (Friedman & Frazier, 2000) from Colorado Children’s found a strong correlation between deep laryngeal penetration and subsequent aspiration in pediatric patients. Most often I find these are infants and children with complex co-morbidities, especially cardio- respiratory.

This discussion is a good one for our self-reflection. It reminds us that the dynamic swallow pathway exists only in the context of the infant or child and what their unique “story” is. Our job is to peel apart the layers of the history, co-morbidities, clinical and instrumental findings, the feeding “environment”, family input, and then thoughtfully reflect on the best plan least likely to cause adverse events. The critical thinking required is built upon organizing our thinking around not only what we know, but what we do not know (or fully understand), which remains quite broad in pediatrics. Those questions become flashlights that we shine into the darkness, allowing us to move forward into the uncertain and unknown thoughtfully. As the philosopher Bertrand Russell once remarked, “In all affairs, it’s a healthy thing now and then to hang a question mark on the things you have long taken for granted”. And so it is, I think, with the work that we do. The “answers” have a way of becoming insufficient or obsolete over time. The questions, the intellectual curiosity, must endure for us to make good clinical decisions for our little patients.

Brooks, L., Liao, J., Ford, J., Harmon, S., & Breedveld, V. (2021). Thickened Liquids Using Pureed Foods for Children with Dysphagia: IDDSI and Rheology Measurements. Dysphagia, 1-13.

Coon, E. R., Srivastava, R., Stoddard, G. J., Reilly, S., Maloney, C. G., & Bratton, S. L. (2016). Infant videofluoroscopic swallow study testing, swallowing interventions, and future acute respiratory illness. Hospital pediatrics6(12), 707-713.

Duncan, D. R., Larson, K., Davidson, K., May, K., Rahbar, R., & Rosen, R. L. (2020).Feeding interventions are associated with improved outcomes in children with laryngeal penetration. Journal of pediatric gastroenterology and nutrition68(2), 218.

Duncan, D. R., Larson, K., & Rosen, R. L. (2019). Clinical aspects of thickeners for pediatric gastroesophageal reflux and oropharyngeal dysphagia. Current gastroenterology reports21(7), 1-9.

Friedman, B., & Frazier, J. B. (2000). Deep laryngeal penetration as a predictor of aspiration. Dysphagia15(3), 153-158.

Gurberg, J., Birnbaum, R., & Daniel, S. J. (2015). Laryngeal penetration on videofluoroscopic swallowing study is associated with increased pneumonia in children. International journal of pediatric otorhinolaryngology79(11), 1827-1830.

Krummrich, P., Kline, B., Krival, K., & Rubin, M. (2017). Parent perception of the impact of using thickened fluids in children with dysphagia. Pediatric Pulmonology52(11), 1486-1494.



Research Corner: Swallowing Biomechanics in Infants with Feeding Difficulties

Variability in Swallowing Biomechanics in Infants with Feeding Difficulties: A Videofluoroscopic Analysis by Laura Fuller, Anna Miles, Isuru Dharmarathn, Jacqui Allen1 (2022) Dysphagia – published online March 2022

This just published paper adds to our evidence and understanding about the dynamic infant swallow.


Clinicians performing feeding evaluations in infants often report swallow variability or inconsistency as concerning. However, little is known about whether this represents pathological incoordination or normal physiologic variance in a developing child. Our retrospective study explored quantitative videofluoroscopic measures in 50 bottle-fed infants (0–9 months) referred
with feeding concerns. Our research questions were as follows: Is it possible to assess swallow to swallow variability in an infant with feeding concerns, is there variability in pharyngeal timing and displacement in infants referred for videofluoroscopy, and is variability associated with aspiration risk? Measures were taken from a mid-feed, 20-s loop recorded at 30 frames per second. Each swallow within the 20-s loop (n=349 swallows) was analysed using quantitative digital measures of timing, displacement and coordination (Swallowtail™). Two blinded raters measured all swallows with strong inter-rater reliability (ICC .78). Swallow frequency, suck-swallow ratio, residue and aspiration were also rated. Variability in timing and displacement was identified across all infants but did not correlate with aspiration (p>.05). Sixteen infants (32%) aspirated. Across the cohort, swallow frequency varied from 1 to 15 within the 20-s loops; suck-swallow ratios varied from 1:1
to 6:1. Within-infant variability in suck-swallow ratios was associated with higher penetration-aspiration scores (p<.001). In conclusion, pharyngeal timing and displacement variability is present in infants referred with feeding difficulties but does not correlate with aspiration. Suck-swallow ratio variability, however, is an important risk factor for aspiration that can be
observed at bedside without radiation. These objective measures provide insight into infant swallowing biomechanics and deserve further exploration for their clinical applicability.

New Shaker Publication: Aerodigestive changes for feeding and swallowing in the neonatal intensive care unit (NICU)

I am pleased to announce my new publication on aerodigestive challenges for preterm and sick newborns who require neonatal intensive care. Supporting safe and successful feeding and swallowing in the setting of aerodigestive co-morbidities requires thoughtful reflection from multiple perspectives, to help us navigate both therapeutic differentials and interventions. The article addresses:  considerations post-extubation, the potential impact of HFNC and CPAP, supporting feeding readiness in fragile infants, stridor, PMV trials, a protocol for NICU infants requiring long-term tracheostomy, and the contribution of instrumental assessment via videofluoroscopic swallow studies. Should be available on the Passy-Muir website soon.

Shaker, C.S. (2022) Aerodigestive changes for feeding and swallowing in the neonatal intensive care unit (NICU). Passy Muir’s Aerodigestive Health Volume 5 Issue 1; 35-42.

Click here to go to Passy Muir website education and download article

Research Corner: Developmental Trajectory of Long-term Oral Feeding Problems in ‘Healthy’ Preterm Infants

Robinson, L., Heng, L., & Fucile, S. (2022). Investigating the Developmental Trajectory of Long-term Oral Feeding Problems in ‘Healthy’ Preterm Infants. Developmental Neurorehabilitation, 1-5.


Purpose: To investigate the occurrence of oral feeding problems in preterm infants up to one year after hospital discharge

Methods: Thirty-six infants born<34 weeks’ gestation were enrolled in a prospective exploratory      longitudinal pilot study prior to hospital discharge. Parents of eligible infants completed telephone questionnaires at 3, 6, and 12 months corrected gestational age. The occurrence and type of feeding problems; medical problems; and rehabilitation services received were collected.

Results: A total of 26 (72.2%) parents responded, with 11 (42%) identifying feeding problems that developed within the first year of life. Avoidant behavior (including crying, agitated/fussy, and refusing to eat) was the most common feeding problem that occurred.

Conclusion: Feeding problems in ‘healthy’ preterm infants may occur at any point in development within the first year of life. Increased screening after hospitalization is needed for early identification and to make appropriate referrals in a timely manner to prevent and/or reduce the severity of long-term feeding problems

Implications for Practice The findings from this study are clinically significant because many ‘healthy’ preterm infants in particular, those born >29 weeks’ gestation, are often discharged from the hospital without specialized follow-up and are not monitored closely for feeding issues by their primary care provider until the problems become clinically significant. Moreover, feeding is reported as a main concern for families of preterm infants following discharge from the NICU and is a major cause for emergency room visits and hospital readmissions to one year after discharge from the NICU. Hence, given the increased susceptibility of all preterm infants to encounter oral feeding problems beyond hospitalization, parental education and counseling should be provided prior to hospital discharge, and infants should continue to be screened and assessed post-discharge

Research Corner: The Effect of Severe Intraventricular Hemorrhage on the Biorhythms of Feeding in Premature Infants

Gewolb, I. H., Sobowale, B. T., Vice, F. L., Patwardhan, A., Solomonia, N., & Reynolds, E. W. (2021). The Effect of Severe Intraventricular Hemorrhage on the Biorhythms of Feeding in Premature Infants. Frontiers in Pediatrics, 870.

Background: Suck-swallow rhythmicity and the integration of breathing into infant feeding are developmentally regulated. Neurological injury and breathing abnormalities can both impact feeding in preterm infants.

Objective: To determine the effects of neurologic injury independent of effects of
disordered breathing on feeding biorhythms in premature infants

Conclusions: We have previously shown that the suck-swallow-breathe rhythms and patterns in preterm infants with bronchopulmonary dysplasia (BPD) differ significantly from those in low-risk
preterm infants (14–18). This has raised the question as to whether the dysrhythmias and abnormal coordination patterns noted in infants with BPD are caused by difficulty breathing
or by the often-concomitant underlying neurological injury commonly seen as co-morbid conditions (such as IVH) in medically complex preterm infants. Neonates with BPD often have IVH or other markers of neurological injury; thus, it is important to differentiate the dysrhythmic effects of neurological injury from any direct respiratory effects of BPD on infant feeding, since a specific “signature” in feeding in infants with neurological issues pointing to a more
vulnerable population would allow resources to be targeted.

Severe IVH has a negative impact on the biorhythms of suck, suck and suck-swallow in preterm infants 35–42 weeks PMA. If a preterm infant with IVH but without BPD at 35–42 weeks PMA
lacks adequate feeding biorhythms, there could be a need for additional workup to identify possibly undetected neurological injury. The independent effect of severe IVH on feeding rhythms
suggests that quantitative analysis of feeding may both reflect and predict neurological sequelae, and perhaps points to a critical period where intervention may be most efficacious.

Problem-Solving: Excessive Rooting in SGA Former 38 Weeker


I work in a level 2 NICU.  We are a small unit with anywhere from 0 to 9 babies at a time.  We don’t often have infants with respiratory compromise nor do we have many infants born prior to 30 weeks’ gestation.  My question is in relation to this population:  premature, occasional resp problems that often are managed and then resolve by discharge.

I had an infant recently with difficulty with getting a proper latch on the bottle when presented.  Infant was a 38 weeker, SGA, initial hypoglycemia, fetal cephalhematoma (no fracture or IVH), and initial hyperbilirubinemia.  He has no known drug exposure and MOB was allowed to breastfeed.  Infant appeared to latch well and was satisfied to breast feed as he would be calm and latch immediately to mom’s breast.  However, since mom’s milk supply was still low, and she was unable to feed every feeding, and infant weight gain was important due to SGA, the infant required bottle feeding.  When presented with the nipple the infant was eager, almost frantic.  Despite palatal placement with gentle pressure the infant continued to root for the nipple.  Nursing reported, “I know that I’m not supposed to use chin support but I did.  I felt like it helped him to find and maintain the latch on the bottle.”  I also noticed that the mother had a similar approach to bottle feeding her infant, also including cheek support.  My approach was to swaddle the infant in a cradled upright position.  Doing that along with palatal placement with gentle pressure as well as providing pressure to the corners of the mouth to increase “feedback” helped on occasion but the feeding was still laborious as this still resulted in a lengthy feeding.  My thought was that, I noticed that when the infant breastfed 1. MOB was so quick that the infant did not have time to work up into a frenzy, 2. infant was well wrapped and contained, 3. the infant mouth and face were receiving pressure against the breast.  I was unable to successfully replicate this for bottle feeding.  Additionally, nursing staff decided to try a faster flow.  I watched the mother feed the infant in an upright cradle position, using cheek support as well.  Initial look on the infant’s face was that the flow was fast, but was able to get into a rhythm with feeding.  So, my question is, is cheek and chin support appropriate in this situation?  What should I try in the future for similar situations of excessive rooting?


You’re doing a good job trying to sort out what is going on. The population in your Level II NICU sounds very typical, mostly GA 30+ weeks and typical respiratory issues associated with preterm birth, that can indeed affect coordination but are not enduring. May often see increased WOB with intermittent tachypnea due to the aerobic demands of feeding. So, breathing regulation is a component we would want to specifically support.

This little guy due to being SGA likely has some challenges with state regulation and can look/get “disorganized” due to more rapid movement to active alert state. One neo years ago told me the altered state regulation in SGA infants is likely related to the increase in catecholamines provoked when one is born SGA that creates this altered state regulation; this then can create poor latch at times, rapid state change to crying, contributing to an ineffective latch and ineffective feeding. Vestibular input (gentle slow rocking, one per second gentle patting to calm the regulatory system) would be important prior to and contingently during feeding, perhaps starting with a few pacifier dips to entrain the oral-sensory-motor system and promote organization without flow at first.

Of course, as you know, “poor latch” can be for so many reasons, sometimes more than one for an infant. Was managing flow rate at breast well but mom’s supply low. Not latching to nipple readily …my first thought is… was the flow from the man-made nipple too fast so he could not organize suck even to start? Or was it hard for him being SGA to transition to a rubber nipple especially if mom’s breasts are larger? Is odd that sensory input to palate (from, I hope, a drained man-made nipple), did not elicit his root-to-latch sequence. Mom likely learned cheek support from the RN – it of course creates flow without active suction/latch perhaps used to “get him infant going”?? But meanwhile he is not learning to establish the motor mapping for an effective root-to-latch sequence for sucking form the bottle—it’s being bypassed. The fast flow nipple selected by RN would be faster than the breast flow – and combined with cheek support and “pressure to the corners of the mouth”, the flow is likely too much, uncouples swallowing and breathing, and interferes with swallow-breathe coordination, in effect provoking less sucking drive and less intake, longer feedings. Agree with secure swaddle for containment and organization, humeral flexion with hands at midline near face. I’d try elevated side lying with capital flexion, eliciting rooting towards midline/towards chin (i.e., into forward flexion) as it can help with organization and support optimal latch by recruiting the proper motor mapping. The infant’s facial expression as if flow was too fast was real, and he might have then tried to accommodate but has limited capacity to do so, which can lead to subtle effects on coordination and likely learning, sometimes maladaptive behaviors.  I suspect with the faster flow there were still subtle occasions of adaptive respiratory behavior such as slight nasal flaring/blanching, slight chin tugging, slight blinking in an attempt to compensate for the faster flow and its impact on the fine coordination of suck-swallow-breathe. No overt events but still a level of physiologic stress, if observed closely. Cheek support would not be helpful based on what I understand about this infant and his presentation. If you see excessive rooting in another infant, focus on “why” that infant with his unique history might be showing that maladaptive behavior and as you unpeel the layers, you will select an intervention clearly mapped to the etiology. Creating flow via a faster flow rate nipple as RNs selected, or passive increase in flow (via cheek support), may be more like band aids, than an etiology-based solution, which I find can be more effective and at the same time promote learning on the infant’s part, with neuroprotection.

I hope this is helpful.

Research Corner: Vocal Fold Movement and Silent Aspiration After Congenital Heart Surgery

Congratulations to our pediatric colleague, Christine Rappazzo,  for this wonderful addition to our evidence base related to the potential impact of the need for heart surgery on airway protection in our infant population. This, combined with the documented increased risk for R vocal fold motion impairment post ECMO in this population, helps us to advocate for our involvement in safe progression to PO for these vulnerable infants.

Citation: Narawane, A., Rappazzo, C., Hawney, J., Clason, H., Roddy, D. J., & Ongkasuwan, J. (2021). Vocal Fold Movement and Silent Aspiration After Congenital Heart Surgery. The Laryngoscope.


Infants who undergo congenital heart surgery are at risk of developing vocal fold motion impairment (VFMI) and swallowing difficulties. This study aims to describe the dysphagia in this population and explore the associations between surgical complexity and vocal fold mobility with dysphagia and airway protection.


This is a retrospective chart review of infants (age <12 months) who underwent congenital heart surgery between 7/2008 and 1/2018 and received a subsequent videofluoroscopic swallow study (VFSS). Demographic information, Society of Thoracic Surgeons-European Association for Cardio-Thoracic Surgery (STAT) category of each surgery, vocal fold mobility status, and VFSS findings were collected and analyzed.


Three hundred and seventy-four patients were included in the study. Fifty-four percent of patients were male, 24% were premature, and the average age at the time of VFSS was 59 days. Sixty percent of patients had oral dysphagia and 64% of patients had pharyngeal dysphagia. Fifty-one percent of patients had laryngeal penetration and 45% had tracheal aspiration. Seventy-three percent of these aspirations were silent. There was no association between surgical complexity, as defined by the STAT category, and dysphagia or airway protection findings. Patients with VFMI after surgery were more likely to have silent aspiration (odds ratio = 1.94, P < .01), even when adjusting for other risk factors.


Infants who undergo congenital heart surgery are at high risk for VFMI and aspiration across all five STAT categories. This study demonstrates the high prevalence of silent aspiration in this population and the need for thorough postoperative swallow evaluation.

This will inform your pediatric practice whether in the inpatient or community pediatric setting.



Problem-Solving: 8 month old with stridor of unknown etiology post VFSS

QUESTION: I would love some advice and guidance. I have a 8 month old that was referred for an outpatient evaluation for feeding/swallowing concerns with a diagnosis of reflux and dysphagia from his pediatrician. Since birth, he has had a persistent stridor as well as reflux. Mom reports having tried multiple formulas, taking Pepcid (as prescribed by his pediatrician) and attempting multiple bottles and nipples prior to finally finding success with Enfamil AR. She reports that only the AR formula has allowed him to gain weight. His BMI was classified as “underweight” at his last appointment with PCP with weight at 20lbs on 6-24-21. The pediatrician recommended that the child see ENT and have a VFSS. No clinical bedside evaluation was conducted first. The ENT saw him in office and recommended a sleep study in addition to the VFSS. The sleep study revealed 4-5 apneic episodes every hour, however, it was ruled as “normal” per parents’ report. They were told that unless he is turning blue then there is nothing to be done at this time. They were very distraught. He wears an owlet, and his mother reports that it goes off continually each night. He is a very restless sleeper. She also reports coughing in his sleep. The VFSS revealed “moderate pharyngeal dysphagia characterized by delayed laryngeal closure resulting in deep laryngeal penetrations with thin (Dr. Brown level 2 nipple utilized) and mildly thick/nectar consistency (Dr. Brown level 3 and 4 utilized) and 1 isolated episode of shallow laryngeal penetration that was trace in volume with moderately thick/honey consistency. Silent aspiration was present with mildly thick/nectar consistency with Dr. Brown level 4 nipple.” It was recommended that he receive all liquids via Dr. Brown Y cut nipple with honey consistency/moderately thick utilized. Specifically, the SLP advised the family to utilize 12ml of Beech-Nut oatmeal cereal to 1 ounce of AR formula. At the time, he was consuming 6-ounce formula bottles so the SLP wrote out for him to consume 72ml of oatmeal to 6 ounces of Enfamil AR (4.75 teaspoons per 6 ounce bottle). He was also encouraged to continue solid age-appropriate diet. Note: Barium was thickening agent utilized during the VFSS and oatmeal not utilized. The flow test confirms this recipe of thickening is greater than moderately thick (honey consistency).

Currently, this child is consuming one 6 oz. bottle every 3 hours. Per his father’s report, he weighs 31lbs. He has gained approx. 10-11 pounds in less than 2 months since his formula has been altered. He is also eating solid cubed and diced foods with no signs or symptoms of aspiration noted. He has to date had no instrumental (laryngoscopy or bronchoscopy) performed with ENT but is scheduled to have completed later this month with ENT citing that he will repair the cleft at that time if present as suspected. I immediately contacted the PCP and requested a dietary consult due to concerns with excessive weight gain and nutrition intake. I’ve also spoken with the ENT to confirm exact plans of scheduled procedure with request to trial a reduction in thickening. The ENT indicated he agreed that he should attempt to decrease intake of added oatmeal.  What would you recommend trialing in office with this child? I want to reduce the amount of oatmeal and thickener utilized as well as aim to alter the nipple utilized to ensure he is as safe as possible pending further instrumental assessment. Thoughts? Advice?


His clinical and radiological presentation are indeed worrisome.  Sounds like etiology for the stridor isn’t fully clear yet. This is, as Laura suggested,  a rather common presentation that often leads to hospital admission (d/t the events like color change that often co-occur) to expedite a workup. ST is often consulted to assist in the differential (neuro vs. reflux vs cardiac  vs swallowing vs airway). These infants are like small puzzles with lots of moving pieces.

I am always surprised and saddened when parents report to me that the stridor and poor feeding are longstanding and unexplained and unsolved for so long. One infant I was consulted on as an inpatient had such loud inspiratory stridor  that I could hear it when I was coming down the hall, and he had suprasternal and supraclavicular  retractions so deep, he could barely move air. Mother recalled the events of color change and need for CPR with tears as she explained his history to me.  The mother was desperate. The infant was so precarious. Long story short, I had to thoughtfully and respectfully advocate for interventions beyond those initially planned by the team that would have mobilized the infant instead to an earlier discharge. At discharge about 5 weeks later,  he finally could breathe and was feeding, and starting to gain motor and developmental function now that breathing allowed. A few months later, on an unrelated hospital visit, the mother saw me across the hospital lobby,  which is huge,  and called out to me.  When I turned around and then came to her side, she hugged me so tight and cried “You saved my baby’s  life, I just know it. I couldn’t have taken him home that way again”. Whew, tears flowed.  In that moment I knew I was supposed to be where I am. There he was, in her arms, doing so well. Those moments stay with you forever. So your thoughtful advocating for this little guy is something I am sure the parents so appreciate, more than you know.

We don’t know anything else about his history, so unsure if something might be relevant. I am also assuming the stridor is inspiratory, which most often co-occurs with laryngomalacia and/or reflux. Expiratory or biphasic stridor would broaden my thinking into other directions. The inspiratory stridor may be related, at least in part,  to the effects of LPR/EER (based on his coughing with sleep, stridor at non-feeding times), but so far,  we have no UGI to provide data about structures/possible malrotations, and we have no scope yet to give us data about potential co-occurring changes in the larynx/airway r/t LPR/EER that might result in decreased laryngeal sensation. If there were, that could be perhaps part of the etiology(ies) for the events of bolus mis-direction and airway invasion witnessed in radiology.

The stridor may also be due to a primary airway problem such as laryngomalacia with or without co-occurring laryngeal cleft, or both EER/LPR and an airway difference. With no laryngoscopy or bronchoscopy by ENT, we don’t yet know. The correlation between laryngomalacia and airway invasion is quite high in the literature. His WOB, often provoked by multiple reasons for stridor, can often dynamically affect swallowing physiology from moment to moment during a feeding. From the swallow study we know that there was delayed laryngeal closure but no other information about swallowing pathophysiology to help us understand alterations along his swallow pathway better.

In the swallow study I wonder what he would have done with first looking at changing nipple flow rate better manage flow rate, prior to moving to thickening. Given the deep LPs with a level 2,  perhaps  could they have trialed a level 1 nipple with co-regulated pacing with Enfamil AR since it has a bit greater baseline viscosity than typical thin liquids, for example. The high level of thickening prescribed may be affected by an artifact, in that a Y cut nipple will always require more thickening given that it is the highest flowing nipple. Thickening to this degree is I think rare because often we suspect that if this level of thinking is required  to establish a “safe” swallow, is there risk during a true feeding of 30″ (compared to 2-3″ under fluoro), when small changes like the infant sucking a little harder or faster , or change in head/neck position, or taking an extra or prolonged breath r/t likely increased WOB, for example , may indeed alter physiology in the moment, and lead to silent aspiration of this quite thick consistency.

It is possible a different nipple flow with less oats could be safe and more supportive of dietary needs, using data you have from the study. Given the deep laryngeal penetrations and events of silent aspiration, without defined etiology (ies), I wonder if it might be worrisome for this infant to make changes in nipple and thickening level outside the benefit radiology, which would provide objective data about the impact of the change on physiology and airway protection. Perhaps try to schedule a repeat study soon, so you can objectify the changes you make with your interval  plan that appear clinically to be helpful.  Minimizing x-ray exposure is of course important; he just sounds precarious.