Shaker Seminars in Phoenix: June 24-28, 2022

Whether you are looking for a solid foundation in neonatal/pediatric swallowing and feeding, or for advanced clinical learning opportunities, my seminars have been designed with you in mind.

Join me for an exceptional learning opportunity in June. Whether you are in acute care or part of a community setting, you will benefit from the latest research combined with my 45 years of experience in neonatal/pediatric swallowing and feeding. Enjoy a collegial environment that fosters interaction and learning along with each other.

Choose from my NICU Swallowing and Feeding and After Discharge course on June 24-25, followed by Pediatric/NICU Video Swallow Studies on June 26th, and then my new Advanced Infant/Pediatric Dysphagia on June 27-28th.

Click here to download Shaker 2022 On-Site Seminars Brochure

Click here to Register

Click here for Lodging and Directions for Phoenix

Hope you can join us!

Feedback from attendees:

“Attending this course is for me as an SLP like playing a new piece of music. I had the individual notes but now I have the melody of the music! Have such a better understanding of many concepts from the levels of evidence base to being ok living in the “gray zone” and problem-solving, to communicating with physicians more effectively. Thank you”! Julie, SLP

“So much real time experience, cases, research to share. Especially appreciated examples of how Catherine educated and navigated challenging scenarios with nurses, physicians and families. Thanks for the research evidence and an amazing learning experience.” Linda, SLP

“I would definitely recommend this course because the information is evidence-based coupled with a speaker with years of clinical experience. Together made for a dynamic conference!” Aimee, OTR

“The seminar will benefit me in every way! Stop doing some things, keep doing some things, start doing some things differently!” Mary, SLP

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.


Research Corner: High Flow Oxygen Therapy and the Pressure to Feed Infants with Acute Respiratory Illness

The impact of Nasal Continuous Positive Airway Pressure (NCPAP) and/or High Flow Nasal Cannulae (HFNC) on swallowing physiology in infants via the swallow-breathe interface is not fully understood. However recent literature is worrisome for increased risk for airway invasion, often silent. It is increasingly common for hospitalized infants to have orders to PO feed while requiring this level of respiratory support. PO feeding is part of the path to discharge.

Some may be otherwise normally developing and recovering from a viral process, yet still present with precarious readiness to return to PO. Some may have a  premorbid history of feeding/swallowing problems, and co-morbidities that place them at an even higher risk. Further research is needed to guide for safe return to oral feeding of infants and children in the PICU with an acute respiratory illness who require NCPAP or HFNC.

In the interim, careful clinical assessment and consideration of risk from multiple perspectives are essential. Conversations with the team that follow will require familiarity with the current literature and dialogue that considers that  infant’s presentation and unique risks. Sometimes, despite our advocacy, there is a decision to proceed with PO feeding. Cautious pacifier dips for purposeful swallows may be followed by brief small PO trials with a slow flow nipple with strict co-regulated pacing to limit the bolus size and support swallow-breathe synchrony, with positioning that optimizes tidal volume. Once there has been some brief motor learning and problem-solving, an instrumental assessment to objectify swallowing physiology under the  current respiratory support would be essential. It is critical that physiology and pathophysiology be our focus in radiology, not just the events of bolus mis-direction in and of themselves that we happen to capture in the short time under fluoroscopy. During the course of a true feeding, intermittent/interval changes in rate and depth of breathing, tidal volume and/or vigor may be a tipping point that leads to silent airway invasion. I don’t know that this is readily understood by all of our medical colleagues.

While my conclusions above differ from those of the authors regarding the potential role of instrumental assessment, the article referenced below is a valuable resource for you:

Raminick, J., & Desai, H. (2020). High Flow Oxygen Therapy and the Pressure to Feed Infants with Acute Respiratory Illness. Perspectives of the ASHA Special Interest Groups5(4), 1006-1010.


Purpose Infants hospitalized for an acute respiratory illness often require the use of noninvasive respiratory support during the initial stage to improve their breathing. High flow oxygen therapy (HFOT) is becoming a more popular means of noninvasive respiratory support, often used to treat respiratory syncytial virus/bronchiolitis. These infants present with tachypnea and coughing, resulting in difficulties in coordinating sucking and swallowing. However, they are often allowed to feed orally despite having high respiratory rate, increased work of breathing and on HFOT, placing them at risk for aspiration. Feeding therapists who work with these infants have raised concerns that HFOT creates an additional risk factor for swallowing dysfunction, especially with infants who have compromised airways or other comorbidities. There is emerging literature concluding changes in pharyngeal pressures with HFOT, as well as aspiration in preterm neonates who are on nasal continuous positive airway pressure. However, there is no existing research exploring the effect of HFOT on swallowing in infants with acute respiratory illness. This discussion will present findings from literature on HFOT, oral feeding in the acutely ill infant population, and present clinical practice guidelines for safe feeding during critical care admission for acute respiratory illness.

Conclusion Guidelines for safety of oral feeds for infants with acute respiratory illness on HFOT do not exist. However, providers and parents continue to want to provide oral feeds despite clinical signs of respiratory distress and coughing. To address this challenge, we initiated a process change to use clinical bedside evaluation and a “cross-systems approach” to provide recommendations for safer oral feeds while on HFOT as the infant is recovering from illness. Use of standardized feeding evaluation and protocol have improved consistency of practice within our department. However, further research is still necessary to develop clinical practice guidelines for safe oral feeding for infants on HFOT.

Problem-Solving: 9-year-old boy with a dx of Myotonic Dystrophy


I have a curious case question to put to you. I just saw a 9-year-old boy with a dx of myotonic dystrophy for a swallow evaluation. However, his mother reports no actual difficulty with swallowing food and liquid, but that he has experienced 4-5 acute episodes of gagging/choking behavior with no oral intake at all, over the last 6 months or so. Apparently, with no liquid or solid material being consumed, he has begun to have episodes where he will cough/gag/choke with such severity that he has difficulty breathing, and it’s very frightening to his teachers/family.

I did a bedside swallow eval and observed very low muscle tone in his tongue, lips and face, but no drooling and no anterior/lateral spillage of bolus textures. There is poor coordination and mastication of solid textures, and often food is swallowed not-fully-masticated, but he showed no s/s of aspiration or penetration with the liquid and solid textures I gave him. I never saw this coughing/gagging behavior today, and don’t quite know what to tell the parents.

My suspicion is that he is aspirating on his own saliva, which does pool in the anterior portion of his oral cavity frequently. But why would this just start to affect him to such an extent, when that has been his baseline for years?

Have any of you heard of this happening with MD? Any ideas a) what is causing the episodes and b) any way to help?


Sounds like there are multiple pieces to this puzzle. The systemic hypotonia both distal and proximal makes me wonder about overall motility and integrity throughout the aerodigestive pathway, both oral, pharyngeal, and esophageal and beyond. The lack of adverse overt events reported by family may be an artifact, given that typically hypotonia and hyposensation often go hand in hand. That may be why, along with a likely delay r/t ineffective supra and infrahyoid function, that he does not sense the excess saliva in his oral cavity which you described. The incompletely masticated foods can then be swallowed, likely pharyngeal constrictors are lax to some degree, and the lack of bolus clearance is not sensed until a sufficient volume triggers the altered sensory system, or it eventually migrates toward the airway post feeding.

The likely co-occurring etiology of esophageal dysmotility (EER/LPR) and/or structural/emptying alterations of the esophagus or lower GI tract, or an outpouching, may also be part of the differential. It’s not uncommon for proximal hypotonia to affect the entire body, which would include motility throughout the GI system. Children with postural hypotonia often are high risk for constipation due to poor GI motility and that can create havoc for digestion, provoke reflux and create or exacerbate maladaptive swallowing and feeding behaviors.

Sounds like a VFSS with UGI and small bowel follow through would be very helpful to explore the aerodigestive pathway and objectify his swallowing physiology. I would not be surprised if results indeed raise concerns about silent airway invasion and multiple competing etiologies. I like Amanda’s idea of then pulling in neurology, as his myotonic dystrophy may indeed be worsening and be another part of your differential.

You are doing a great job sorting out a very complex presentation. Our kids like to keep us thinking outside the box.


Research Corner: Infant and maternal factors associated with attainment of full oral feeding (FOF) in premature infants

This newly published paper reminds us that, in the NICU, care is best when it is family-centered. Our most vulnerable preterms and their mothers benefit most when compassionate and thoughtful caregivers consider not only the infant’s co-morbidities but also maternal anxiety, stress, and depression, when assessing premature infants’ oral feeding performance. They influence each other, and should guide our approach to supporting the feeding experience.


Muir, H., Kidanemariam, M., & Fucile, S. (2021). The Impact of Infant and Maternal Factors on Oral Feeding Performance in Premature Infants. Physical & Occupational Therapy In Pediatrics, 1-7.


Aims: To identify infant and maternal factors associated with attainment of full oral feeding (FOF) in premature infants.

Method: A retrospective study was performed on 89 premature infants (<34 weeks gestational age) from a tertiary care neonatal intensive care unit (NICU). Infant and maternal factors were concurrently assessed. Infant factors included gestational age, birthweight, continuous positive airway pressure assistance, mechanical ventilation support, and presence of neonatal morbidities including bronchopulmonary dysplasia (BPD), necrotizing enterocolitis (NEC), and intraventricular hemorrhages (IVH). Maternal factors included maternal age, first born, twin birth, and presence of mental health conditions including anxiety, stress, or depression.

Results: A total of 89 premature infants were included in the sample. A stepwise linear regression model revealed that infants who received mechanical ventilator support and presence of maternal mental health conditions were significantly associated with time to attain FOF.

Conclusions: Results suggest that oral feeding performance is influenced not only by infant’s medical severity denoted by need for ventilator assistance, but also by presence of maternal anxiety, stress, and/or depression.

Details of conclusion: In terms of infant factors, this study revealed that mechanical ventilation support is associated with time to attain FOF. These study results are supported by others who found that infants with a chronic lung disease who require oxygen therapy or prolonged ventilation, are older by post conceptual age, when bottle feeding is initiated. Although the literature indicates that younger gestational age, lower birth weight, and neonatal morbidities such as BPD, IVH, and NEC are associated with longer FOF attainment these factors were not significant in this study. The lack of significance in GA, BW, and neonatal morbidities is likely because both infant and maternal factors were simultaneously assessed in the stepwise linear regression model which may have impacted the significance of these variables on FOF. Stepwise linear regression model essentially does multiple regression a number of times, each time removing the weakest correlated variable. At the end, the variables remaining are those that best explain FOF. Oral feeding consists of infants’ ability to generate and coordinate suck, swallow, and breathe processes. This entails proper functioning of the oral musculoskeletal, cardiorespiratory, and gastrointestinal systems. Taking the above into consideration, the study findings suggest that infants’ respiratory status, defined by need for mechanical ventilation assistance, has a significant effect on FOF, as it is one of the main systems involved in the oral feeding process. With regards to maternal factors, this study found that the presence of a maternal mental health condition, in particular anxiety, stress, or depression, is negatively associated with attainment to FOF, which corroborates a recent study (Park et al., 2016*). They found that increased maternal psychological distress was associated with decreased use of developmentally supportive feeding behaviors. These results suggest that mothers with psychological distress may be less responsive to the infant signals and needs. The literature suggests that maternal mental health conditions are associated with feeding behaviors but does not directly link this factor to delays in FOF as in this study. The study findings bring to light the importance of considering both infant and maternal factors when assessing premature infant’s oral feeding performance. 

*Park, J., Thoyre, S., Estrem, H., Pados, B., Knafl, G., & Brandon, D. (2016). Mothers’ psychological distress and feeding of their preterm infants. American Journal of Maternal Child Nursing, 41(4). Available through Google Scholar


Problem-Solving: NICU Baby with pharyngeal stasis post-swallow on swallow study


Is there any particular intervention improving pharyngeal clearance with the swallow. This infant has pharyngeal stasis post swallow on the swallow study. Diffuse residue, hard to quantify as it varied throughout the study, but definitely not a little…enough that poses a risk for aspiration post-swallow/as feeding continues. UES opened for a portion of the bolus to pass through, pharyngeal stripping was not great. No nasopharyngeal regurgitation that I recall. Reasons for the swallow study were bedside symptoms of desaturations during oral feeding at ~37 weeks PMA and a steady decline in his oral intake & feeding cues. Some background: He is an ex 33-weeker, now 39+5. Questionable dysmorphic features, we are awaiting genetic testing results. ENT did not find any structural issues, but his cry is described as “quiet” by nurses. Early on in my assessment (maybe ~35 weeks) I couldn’t elicit a tongue-lateralizing reflex, haven’t checked since. He also has a high palate and often is nasally congested. Recent ECHO showed a moderate ASD. Recent hearing test indicates possible sensorineural loss, but they want to re-do it. He also gets very constipated. Overall low energy and alertness for his age. All signs seem to be pointing to a neurological basis for his dysphagia and I’m just wondering if there are any last hail marys to try before we start to plan for home on NG, OP feeding therapy, etc. We put him on an oral rest for now. I’ve talked with team and parents both about aspiration risk and oral feeding aversion. Medical team is very supportive of therapy. Any ideas are greatly appreciated!


Thanks for such a detailed history to help to consider possibilities. Not an uncommon presentation that can go many directions as further data comes in.

I like to start with the whys to guide intervention options. Multiple co-morbidities at play it seems. The dysmorphic features stand out as worrisome, and often craniofacial and cardiac variants like an ASD can co-occur. None of the clinical or physiologic behaviors can be attributed strictly to being born preterm, though preterm birth would increase risk for co-morbidities. When I read your post with such  clear  clinical and radiologic presentation,  the possible etiologies/questions that popped in my mind as I read your post were: hypotonia (constipation, lethargy, oral-motor disintegrity understood thus far; wonder about postural control and movement patterns, sensory-moor function include trunk and head/neck), extra esophageal reflux (nasal congestion, lax pharyngeal constrictors, perhaps postural hypotonia), poor posterior driving force of tongue (often correlated with hypotonia, poor pressure generation  to help achieve UES relaxation and opening, posterior tongue tie and/or mandibular hypoplasia….seems at times ENTs miss that…). The quiet cry may suggest retracted tongue (? for stability and/or  r/t tethered oral tissues, r/t mild mandibular hypoplasia). Wondering about work of breathing, swallow-breathe interface with both pacifier dips and/or clinical observation of PO feeding. Has there been a neuro consult? MRI brain? Genetics consult? OT consult? Likely at risk for bolus mis-direction from below (refluxate), d/t what sounds like proximal hypotonia that could make  timely effective response to retrograde flow from the esophageal body unreliable.

All the etiologies that I mentioned, in isolation or in combination, could play a part in the diffuse pharyngeal stasis/residue observed, which is worrisome for bolus mis-direction during the course of a true feeding. I am surprised there was not retrograde flow into the nasopharynx (what some describe as nasopharyngeal regurgitation), given the diffuse residue. Pacifier dips in a secure swaddle elevated side lying position would allow for purposeful swallows and motor learning yet reduce risk for airway invasion, given that etiology is not fully clear. The motor learning from the pacifier dips would keep him learning but minimize risk.

What we know so far suggests a poor prognosis for being a full PO feeder at time of d/c from the NICU and the etiology(ies) is/are unlikely to resolve in the short term, given multiple complex co-morbidities, as yet not fully determined. As a result, pending further data, they might consider a G-Tube with a Nissen  (to optimize airway protection and more safely buy him time for response to therapy and evolution to guide the differential), instead of home NG, which would have its own attendant sequelae.

Search google scholar for this  article by my colleague and friend, Laura Brooks, which may or may not be pertinent, pending your further assessment and refection. Her paper is one I reference with neonatologist’s and intensivists when indicated.

Brooks, L., Landry, A., Deshpande, A., Marchica, C., Cooley, A., & Raol, N. (2020). Posterior tongue tie, base of tongue movement, and pharyngeal dysphagia: what is the connection?. Dysphagia35(1), 129-132.

Abstract: Ankyloglossia, or tongue tie, and its impact on the oral phase of feeding has been studied and debated for decades. However, the impact of posterior tongue ties on the pharyngeal phase of swallowing is not well documented in the literature. A videofluoroscopic swallow study (VFSS) allows for visualization of the oral, pharyngeal, and esophageal phases of the swallow. When decreased base of tongue movement, impaired pharyngeal pressure generation, and presence of pharyngeal residue are noted during a VFSS, a neurologic etiology can be suspected. However, in the setting of a normal MRI with normal motor development, other etiologies need to be explored. If it is not neurologic, could it be anatomic? We present a 21-month-old patient with significant pharyngeal phase dysphagia which was most saliently characterized by impaired base of tongue movement, poor pressure generation, and diffuse residue resulting in aspiration. He was eventually diagnosed with a posterior tongue tie and underwent a frenulectomy. Results via subsequent VFSS revealed significant improvement in base of tongue movement, pharyngeal pressure generation, and pharyngeal constriction, resulting in efficient movement of the bolus through the pharynx into the esophagus, no nasopharyngeal regurgitation, no aspiration, and near resolution of his pharyngeal dysphagia. Patients with impaired base of tongue movement and impaired pressure generation resulting in pharyngeal residue in the setting of a normal neurologic workup could possibly present with a posterior tongue tie which should be examined and included in the differential diagnosis.

I hope this is helpful.