Problem-Solving: 30-month-old with Random Gagging and Altered Swallowing Physiology

QUESTION:

Recently, I completed a MBSs on a 30-month-old child secondary to complaints of vomiting, gagging/choking at random. At age 24 months, child had tonsillectomy/adenoidectomy completed secondary to vomiting/gagging with the hopes this would correct child’s difficulties. MOC reports that this did help some however reports difficulties have not completely resolved. Per MOC, child had pacifier until age of 20 months. At time of MBSs child did consume pureed and thin liquids, they refuse all other bolus consistencies. Child noted to have a high palate arch and slightly narrowing in front of mouth. Delayed swallow to the level of the pyriform sinus was observed, suspect secondary to poor retraction and elevation of tongue to soft palate due to high arch. No penetration or aspiration noted. Appropriate ROM with tongue was observed during attempts at oral facial/motor examination. Per MOC, child is a picky eater, consumes 30oz of milk daily, will pocket food and spit it out and gag on water intermittently.

Based off of how this child presents, I would focus on lingual strengthening, age-appropriate mastication patterns and acceptance of age-appropriate foods. For a child of this age, what would your recommendations be for treatment/tasks to obtain these goals/exercises etc.? I am running into a roadblock per say. From my research and reading, I have found great ideas for older children or adults who follow verbal directives, however due to this child’s age, I am stuck!

ANSWER:

Is the child otherwise normally developing? Is postural /sensory-motor control age-appropriate?  I am asking because sometimes this type of clinical presentation is part of a bigger sensory processing issue or part of a constellation of craniofacial alterations or alterations across developmental domains. That creates a different “bigger picture” from which to problem-solve.

Craniofacial malformations often co-occur with changes in the muscular network that supports those structures. The high arched (and sometimes “tented”) palate can co-occur as part of a genetic syndrome and can co-occur with mandibular hypoplasia. Mandibular hypoplasia alters lingual and supra/infrahyoid muscular ROM and their functional coordination.

Interestingly, I have seen across the age span that, with this clinical presentation you described, it is not uncommon to have co-occurring tethering of oral tissues. I suspect that, if there are TOTs, this may be because the formation of these structures and muscular attachments occurs around the same time in utero. Then their motor sequences are initially mapped in utero through swallowing of amniotic fluid. So, the underpinnings for a well-integrated oral-motor system are underway quite early. Maladaptive networks also start in utero and the foundations for function can then start off in infancy already altered and impact future function that “feeds forward”, as our PT colleagues call it, in motor learning. So, implications unfold overtime.

If there are tethered oral tissues, or related alterations, they can at times be more subtle. These alterations can create challenges for the emergence of motor plans along the swallow pathway, and for bolus control and manipulation. That may also provoke the air swallowing that can lead to the vomiting/emesis you report. We must of course recognize that tethered oral tissues are not always the explanation/etiology, but should be a part of your thoughtful differential, as it could explain the functional limitations you describe. As could altered oral-facial tone, an altered overriding postural network, and/or sensory integration problems, and other possibilities, depending on the unique “bigger picture” for this child. Thinking through that bigger picture will best guide targeted interventions.

A wonderful resource on the neurodevelopmental underpinnings for feeding development is included in Robyn Walsh and Lori Overland’s book on “Functional Assessment and remediation of Tethered Oral Tissues”. Even if TOTs are not part of this child’s etiology(ies), their tutorial included in their book is not just about TOTs but is a foundational must read on functional oral motor development. By two of our wonderful SLP colleagues.

The swallow study would likely reveal any alterations in base of tongue retraction and pressure generation that may be created if tethering were impacting this child’s swallow pathway. For some children, the oral phase appears most altered, but that of course can cause problems down the line such as gagging and “sudden” loss of control which mother describes, which may reflect challenges with coordination during the dynamic swallow (when the need for exquisite motor mapping is required).

The attached article by my colleague Laura Brooks that adds to our understanding of the potential implications of some of the potential alterations. Even though with your patient there was no witnessed airway invasion, there was an alteration in physiology that likely is connected somehow to the functional differences you are seeing. This may take some peeling apart layers of data through a second and third look. Or more. And it may take a while to sort out and trial the interventions that best meet your differential. And that’s ok. It’s complex but you have a good start.

Click here for Laura Brooks article

Practicing at the Top of Your Profession in Feeding/Swallowing

An SLP asked recently, “What resources, articles, courses, etc. did you find helpful when you were first learning infant feeding? I’m looking for something to give me what I really need.”

“My seminars” I told her, “are designed to do just that. When I created them, and as I update them, I always think ‘What do I wish I had known, both research and clinical information, to practice in peds dysphagia when I started out? What is essential to work toward practicing at the top of our professions?’  My NICU and Pediatric as well as Advanced seminars, my Peds/ Neonatal Video Swallow Studies and Cue Based seminars are filled with everything I want to pass along. As I learn from colleagues and attendees at my courses, I weave that in as well. Sometimes I almost run out of time!

I will always offer you a welcoming environment that fosters interaction and learning along with each other.

Click here to download Shaker 2022 On-Site Seminars Brochure

Click here to Register

 

Problem-Solving with Catherine: Navigating Acute Care/PICU Practice Challenges

QUESTION: I am working with a team of non-dysphagia specialists because of shortage of SLP (not in the USA) in pediatric ICU (PT, nurses). When I arrived, I realized that they do everything wrong in SLP standards : start dysphagia exam too early on, speed dysphagia bedside exam with a bit of water, rely only on coughing to assess if dysphagia is present or not, do not do a single swallow FEES/VFSS, do not even know/care about silent aspiration, progress up very rapidly through textures when mastication is not yet possible in my opinion, give rapid directions to families and do not overwatch. Of course, they refer to SLPs for complicated cases, they are scared with or when they are unsure. We are left with the slowly recovering kiddos. they simply judge by overall recovery. If overall is fine, dysphagia is fine for them. But I feel they would be more complications in the adult population however with this type of approach. I am starting to question my stance on dysphagia eval among children in ICU. Is it way simpler than we may think? Do you have an opinion?

ANSWER: I would continue to use the evidence base as your guide, combined with your clinical expertise. Our PICU patients are often fragile but the adverse response to decisions or approaches that are not consistent with best practice may be silent, may increase need for respiratory support without adverse overt events and the child may “run under the radar” for a while. That doesn’t mean you abandon your critical thinking. Not sure if this is a travel assignment or they are the newly added team members, but you will need to decide how best to advocate for your peds patients and to reconcile this risk. That means perhaps having a conversation with them that is respectful, offering practice guidelines by ASHA or research evidence, thinking about how to gain administrative support to foster collaboration and best practice in dysphagia, and what your next steps will be to assure there is appropriate care and colleagues “do no harm” which you likely have an obligation to address via risk management. Should something adverse occur and there is litigation, your documentation and whether it and your actions were consistent with best practice would be scrutinized and determined by an expert pediatric acute care SLP. Always manage patients and document as if litigation is possible, because it is. Trust your instincts. It’s a really challenging situation but best to take control of it in one way or another versus being a bystander when it may affect your professional practice and patient long-term outcomes. That may indeed be leaving if the risk to you is not acceptable, which is clearly possible based on what we know. I hope this is helpful.

 

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

ANSWER:

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

QUESTION:

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!

ANSWER:

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

Question:

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?

Answer:

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). https://doi.org/10.1007/s00455-022-10433-5

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?

Question:

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?

 

Answer:

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.

 

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.

 

 

Problem-Solving: Excessive Rooting in SGA Former 38 Weeker

Question:

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?

Answer:

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.

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?

ANSWER:

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.

 

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

Question:

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?

Answer:

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.

 

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

QUESTION

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!

ANSWER

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.

 

Problem-Solving: Use of Cheek Support in the NICU – The Bigger Picture Beyond Volume

I wanted to share this question posed to me by  Suzanne Evans-Morris PhD, SLP. One of my mentors early in my career as a pediatric SLP, she is amazing. Her key teachings about the postural mechanism and sensory-motor learning that underpins feeding and swallowing are foundational. You can reach her through her website,   www.New Visions.com. My favorite place on her site is the section called “Feed Your Mind”. Reinforces the importance of each of us being a lifelong learner !

Question:

If an infant has an inefficient suck because of lack of buccal fat  pads and often slightly low tone the combination can result in too wide a jaw excursion and a very inefficient suck.   Why would you not give jaw and cheek support (as needed) to make the whole coordination process easier and less fatiguing?  If the baby’s resulting suck, then,  is strong enough to receive too fast a flow, I would think that the solution would be to use a nipple with a slower flow rate, not eliminate the support that improved the suck.   If nurses are giving too much support, it would also help to provide the training to create guidelines for the amount of support that is just right for each infant.

Answer:

With all of our NICU babies, the value or adverse effect of strategies requires consideration of a number of underlying and related issues. One must consider the whole infant, i.e.,  co-morbidities (respiratory, airway, sensory-motor, and GI) when looking at supportive/compensatory techniques for feeding/swallowing.

Sucking pads are believed to develop in the last month of intrauterine life, so approximately 36 weeks in utero. They are not available to many preterms. In normal postural/oral-motor development, the cheeks and lips are not fully active (i.e.,  not the key driver) for feeding in the normal newborn until 3-4 months of life. Prior to that time, the cheeks/lips (they work as a system) posture on the nipple/breast for stability–they do not actively form an anterior seal to obtain the fluid bolus. As a result, the nutritive suck is achieved through a strong “tongue-palate” seal. I have seen a couple newborns and preterms with, unfortunately, multiple hemangiomas that eroded the cheeks and lips right after birth; each was able to feed effectively (no cheek support needed) due to an intact tongue and palate, and, therefore, a tongue-palate seal.

Even with a slow flow/controlled flow nipple, our vulnerable preterms can get too much flow, too large a bolus. When we add cheek support, we will increase the flow rate and the bolus size. Because most preterms have very strong sucks, often too strong for their own good, and are “stuck in sucking” much of the time, as Pamela Lemons wrote, caregivers must look at the dynamic, or synactive, impact of  all interventions on each other. If cheek support is used, it affects more than the suck, in other words.

Increasing the flow rate, or doing so inadvertently through cheek support, is not supportive for preterms’ swallowing safety. While it will increase intake (efficiency of feeding), it is likely to result in physiologic instability. This may or may not be apparent as aspiration events in preterms are most often silent in my clinical experience. The anatomy of the preterm and the physiology of the swallow predispose the infant to easily overfill the valleculae; this, combined with a tendency toward increased work of breathing and an increased respiratory rate, along with neuromotor and neurologic immaturity, can render the airway unsafe. The preterm is unlikely to be able to make the dynamic adjustments required as the pharynx reconfigures itself from a respiratory tract to an alimentary tract  and back to a respiratory tract with each swallow, especially if it occurs in the presence of flow that may readily move to a rate beyond his capacity.

We can provide the postural stability to offset lack of sucking pads through effective swaddling with limbs to the body midline, elbows inside the blanket, an elevated sidelying position, neutral head neck flexion with slight tilting down of the chin.  Using this infant guided approach, via offering a slow flow nipple by eliciting the infant’s active rooting response,  is followed by  contingent co-regulated pacing and resting,  based on the infant’s continuous feedback to help suck, swallow and breathing remain coupled and synchronous.

I have  observed preterms offered cheek support during a Video Swallow Study (to assess its impact on the swallow, as it was being used at bedside by well-intentioned caregivers). They were observed to typically overfill the valleculae and penetrate or aspirate as a result. Matthews wrote years ago that, with preterms, it is not the work of “sucking” that makes feeding challenging but the work of trying to “breathe” in the presence of a flow they cannot manage safely, which in turn then inhibits/disrupts breathing.

If volume is the overriding goal, cheek support may be viewed as a critical tool by some caregivers, and often unfortunately is.  With continued progression toward true infant-guided feeding, and away from volume driven feeding,  the reasoning behind not using cheek support for preterms will hopefully be more readily understood by our nursing colleagues. Until then, learning along with our nursing colleagues while we feed infants will open up discussions about the “why” behind our protective strategies, and the impact of well-intended volume-driven strategies on swallowing physiology and neuroprotection.

 

Follow up commentary from Suzanne Evans Morris:

Catherine,

Thank you so very much for your detailed commentary looking at the interacting factors affecting a premature infant’s coordination of suck-swallow-breathe, and the negative impact that providing external jaw/cheek support can play.   It was so clear, and I have learned a lot.

Suzanne

Suzanne Evans Morris, Ph.D.

New Visions

 

Problem-Solving: Laryngomalacia in Level 2 NICU Infant

QUESTION: I am currently seeing a full term baby in our level 2 nursery. She has an inhalation stridor. At times her stridor is quiet & other times very loud. She had a fees completed & the ENT noted a minor laryngomalacia ; he also reported it was so minor that it should not effect feeding but is causing reflux. She is only takes under 7 ml at each feed the rest is through her ng. We have noticed a decrease in her oral feeds last week she as taking over 49% PO & now less then 20%. I suspect shut down. She is being held semi upright & side lying , using Dr Brown preemie nipples & being paces at 4. Which is very conservative. she is also disorganized with her latching. She will latch then suck 2-4 then push the nipple out of her mouth & also some of the breast milk. She does desaturation down to 86 at times during her feeds – hence the strict pacing. We don’t have infant VFSS at our hospital & the ENT did not see her take a bottle during the fees.
I am thinking we should have her transfer her to a NICU to get a VFSS but I honestly don’t know.

ANSWER:

I think you are correct to be concerned. Her behaviors are worrisome, especially given that multiple papers have associated LM with airway invasion in infants. A google scholar search will yield several.

The dynamic adjustments of the airway surrounding the swallow create the perfect storm for airway invasion, often silent, in our little ones with LM. The infant’s behaviors
(“disorganization” that may indeed be purposeful due to not wanting to suck in order to protect herself, limited drive to feed – purposeful – to stop the experience and/or due to the effects of increased WOB, pushing the nipple out likely to stop the flow which may be being mis-directed, desaturations which have been correlated in the research with aspiration in some NICU infants and is potentially suggestive of insufficient depth and frequency of breaths which would be common with LM).

On an interim basis I would consider an ultrapremie nipple to add even more protection by reducing bolus  size and affording even more support toward our interim goal of sufficient and timely breaths, as we wait for VFSS. Impact of interventions and their combinations could then be objectified in radiology. More strictly pace her, i.e., single sucks, or 1-2 sucks max to proactively further limit bolus size and hopefully increase coordination for now.  If  she is pulling off the nipple after at times 2 sucks, she is telling you that even 2 consecutive sucks are beyond her capacity to manage – either related to bolus size delivered and/or need for a breath sooner then every 2 seconds. Perhaps limit PO trials to with you only for now, unless  there is  no risk for well-intentioned focus on volume by caregivers.

An instrumental assessment will be critical not just to determine if she is aspirating, especially given that radiology is only a moment in time,  but more importantly, to objectify her dynamic swallowing physiology, and the impact of interventions. My clinical experience has been that many of our NICU infants with LM, even those without multiple co-morbidities,  are silent aspirators.

I find it is not uncommon for ENTs and neonatologists to not connect LM with risk for airway invasion and our results in radiology are often unexpected when we share them. Good critical thinking. Trust your instincts with these little ones and continue to listen to their communication just like you did.

My colleague, Ramya Kumar MS. CCC-SLP, BCS-S, CNT, IBCLC, NTMTC mentioned consideration of trialing alternative side down with elevated sidelying, as she has seen under FEES that infant’s with stridor often have arytenoid prolapse which seems to be more dominant on one side vs the other for some reason. That makes so much sense anatomically. Gravity can surely be a friend or a foe to our little ones.

 

 

 

Problem-Solving: Reflux Medication Administration in the Setting of Aspiration

Question

I have an ex-preemie (now adjusted 40 weeks) being worked up for laryngeal cleft – aspirated thins on swallow study even with Dr. Brown Ultra Preemie, but is doing ok with mildly thick liquids for PO; however, he is also on Prevacid and the nurses are mentioning he’s sounding congested when they administer the med (likely aspirating med as it’s not mildly thick consistency).  I typically add other meds to a little bit of the thickened formula to solve this issue; however, Prevacid has to be given on an empty stomach so mixing with formula doesn’t seem to be a good option.  Any suggestion on how to thicken a med that has to be given on an empty stomach?  Also he’s an ex-31 week preemie with a history of r/o NEC, so Simply Thick is not an option

Answer

The onset of congestion with the meds administered unthickened is potentially more worrisome in some ways than aspirating the feeding, from a pulmonary perspective.

You don’t indicate the aspiration was silent in radiology, but he may be at risk for occasions of silent aspiration, given that EER/LPR may be part of the differential and alter laryngeal/tracheal sensation. His potential respiratory issues as a former 31 weeker may add further risk, in the setting of the possible laryngeal cleft. It is possible the audible congestion, especially if it is heard “in synch” with inhalation/exhalation after administration of meds,  reflects airway invasion.

As I understand the limited history above, it sounds like there is no NGT access or they’d be using that for meds. As we consider the relative the risk-benefit ratio for this infant with his clinical presentation, then the risk for airway invasion of the med being offered unthickened is likely going to outweigh the benefit of delivery of the unaltered Prevacid to the gut prior to PO.

Most of the time, while 30″ prior to feeding is recommended for Prevacid administration, the nurses often give the GI meds just prior to feeding to avoid waking the infant earlier. So, it’s unclear to what extent most NICU infants can really take advantage of the time period prior to PO that likely affects positive impact of Prevacid. If the nurse is indeed waking him early to PO, I think the risk-benefit ratio for this infant that I described above still should be considered.

Since you have objectified an apparently approved thickener deemed safe if radiology for swallowing/feeding, I would use perhaps 5mls of that to offer the Prevacid before PO. Is that a perfect solution? No, but it is likely most protective of pulmonary function at this time, based on what we know. In related conversations with our pulmonologists and GI docs, this is the kind of critical thinking have heard them model and that I am fortunate to be exposed to.

His top priority seems right now to be airway protection at this point in the workup, based on data gathered. Reflux may indeed be part of the differential for management, and potentially contributing to his aspiration, but it may have to be a secondary priority at this time, for now.

Perhaps have a conversation with the MDs about their thoughts on the risk-benefit ratio for this infant. Physicians are used to living “in the gray zone” and weighing risk-benefit ratio, so it will be a familiar approach for them, and open the door for collaboration.