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.

 

Problem-Solving: Laryngeal Penetration during Pediatric VFSS

QUESTION:

Some of the SLP’s completing VFSS in the pediatric population are making recommendations solely on penetration. If the child penetrates they assume they will aspirate (due to gravity) and downgrade them to the thickest liquid they don’t penetrate or aspirate with. The reports I have received have not mentioned whether the infant attempts to cough or clear the penetration. I frequently complete fees with the adult population, but my experience is more limited with the pediatric/infant population. Adults will penetrate and clear independently with additional swallows or throat clear/cough to remove the penetration before they aspirate. I’ve also seen flash penetration in adult VFSS does that happen with infants?. I would love some opinions to help guide my practice.

ANSWER:

Infants and children aren’t little adults in so many ways, especially when it comes to swallowing. I’ll share some of the concepts that have influenced my practice and are part of my passion when I teach my seminar about pediatric/neonatal swallow studies.

One of them is that laryngeal penetration, when witnessed,  doesn’t exist in a vacuum. Dr. Coyle has taught us that the significance of penetration, even in the adult population, is on a sliding scale. I love that. He is always so descriptive. I think he means that we have to make decisions on a case-by-case basis, by combining all available information, there is no one size fits all analysis and plan. Then we develop a management algorithm for that patient, with unique co-morbidities, risk factors, history and so on. Each infant/child is unique in birth history, feeding history, postural, sensory-motor, aerodigestive, neurologic status and caregiver attributes. Combined, they all can affect not only what we might witness in radiology but how the infant/child may respond, compensate, or  be affected, and from moment to moment. For example, for our infants, their respiratory co-morbidities will increase the risk for airway invasion, especially under the “right conditions” (i.e., interval change in sucking rate or strength, change in RR or WOB, caregiver artifact). Data analysis in radiology must consider the unique algorithm best for that infant/child based on the available data and understanding of the implications in that context/setting. An otherwise normal infant/child would very likely have a different algorithm after radiology.

Our data set in radiology is limited in so many ways. We must look at the data gathered and focus on the physiology; impressions may be tenuous. We cannot focus on just the events of bolus mis-direction in and of themselves.  A swallow study really is only a moment in time. Bonnie Martin Harris has told us that “aspiration or penetration is neither sufficient nor necessary for a swallowing impairment”. Dr Coyle describes the swallow study as an analysis of how and why the abnormal bolus flow occurred. The alterations in or impairment of physiology, and why that infant/child penetrated,  must influence our critical thinking, and must inform our plan.

All events of laryngeal penetration are not alike in children, and that influences our analysis as well. Their frequency and depth, in the setting of the co-morbidities and age and pulmonary health, are important factors. Friedman and Frazier (2000) found that of those infants/children with witnessed deep laryngeal penetration, 85% went on to aspirate when the swallow study was extended. This correlation between deep laryngeal penetration and aspiration is an important consideration in our “bigger picture” analysis with infants and children. Duncan et al (2019) concluded that laryngeal penetration may be indicative of aspiration risk in children less than 2 years of age. It is also associated with negative clinical outcomes (Gurberg et al, 2015, and Duncan et al, 2019). Duncan’s group concluded that “Any finding of LP in a symptomatic child should be considered clinically significant and a change in management should be considered”.
Another consideration and a key one is what we understand about the evolution of swallowing physiology from infancy toward adulthood. It is closely intertwined with, and highly influenced by, evolving structural relationships of the head/neck, development of maturing postural control and the musculoskeletal network that underlies hyolaryngeal function. At different points along that developmental trajectory, the components of swallowing physiology that guide bolus flow evolve in synch with a gradually more adultlike postural mechanism. Along the way there is: encephalization, sensory-motor learning, skeletal changes, and growth of the larynx. (Ruark, 2002; Gosa, 2013, Riley et al, 2019) At various times along this continuum, physiology is evolving and thus the need for all the considerations I have mentioned about above. This evolution truly is delicate ballet and can be precarious at times. Normal infants and children adapt, and this evolution happens behind the scenes, unnoticed, giving the sense that it happens effortlessly. Not so for the infants and children who land at our doorstep whether in in radiology, early intervention, the outpatient clinic, or our children’s hospital.

Unfortunately, due to adverse effects of radiation exposure, we don’t have data across a wide range of normal infants/children to delineate the variation in pediatric swallowing physiology that may represent normal variation. So, we must peel apart the layers thoughtfully and carefully as each piece of data is obtained.

Perhaps have some dialogue with the SLPs you mention who have sent you reports, so you can learn along with them. Thickening is not always the best intervention either in adult or pediatric dysphagia, and at times may indeed create more risk. That said, some still see thickening as the go-to intervention and yet there may be other or better alternatives for a particular infant/child. There may not be. Have a conversation with that therapist about her/his impressions, rationale, and selection of interventions, and review the study together if possible. That would help build your own understanding of the unique considerations specific to the infants and children you may be following and will build a relationship for future collaboration.  As therapists, we often need to live in the gray zone, as I like to call it, where questions are more common than answers and the answer is rarely straight forward, but that is also the pathway to being a lifelong learner.

I hope this is helpful. Thanks for reaching out.

Duncan, D. R., Larson, K., Davidson, K., May, K., Rahbar, R., & Rosen, R. L. (2019). Feeding interventions are associated with improved outcomes in children with laryngeal penetration. Journal of pediatric gastroenterology and nutrition68(2), 218-224.

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

Gosa, M. (2013). Infant Airway Protection Mechanisms During Swallowing. Perspectives on Swallowing and Swallowing Disorders (Dysphagia)22(4), 156-160.

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.

Riley, A., Miles, A., & Steele, C. M. (2019). An exploratory study of hyoid visibility, position, and swallowing-related displacement in a pediatric population. Dysphagia34(2), 248-256.

Ruark, J. L., McCullough, G. H., Peters, R. L., & Moore, C. A. (2002). Bolus consistency and swallowing in children and adults. Dysphagia17(1), 24-33.

 

 

 

Problem-Solving: Duration of utilizing side lying positioning for feeding

QUESTION:

I haven’t found anything specific in the literature, but I cannot think of a rationale for ceasing a sidelying at 4 months of age.  I heard this at a course. I nursed all 4 of my own children until they were around 1 year of age, which means that they were in  sidelying (each side) during feedings for 1 year.  I also find that if a baby with an intact sensory system has the drive to resist a side lying feeding position,  then they are likely no longer in need of that protective positioning.  I did read the abstract to the systematic review that was done by Park, Pados and Thoyre, but since I didn’t have access to the full article, I can’t swear that a timeline was not referenced, but it wasn’t suggested in the abstract.  If the parent is capable and the baby accepts, I will have the parents feed from both sides if they are capable and steady and the baby will accept it, being mindful of vision development and head shape.  I am curious to know your thoughts on the matter.

ANSWER:

For me it is all infant-guided. I let the infant tell us. There is no arbitrary age for anything really, it is based on developmental readiness for a change, less need for a support.  I suggest parents trial a more typical feeding position when infant has been home for a month or so and has been feeding without stress in a sidelying position.  If the infant feeds as well in the new position as he did in sidelying, then the infant is telling you he is ready for the new position. If he does not feed as well in the new position, he is telling you he is not quite ready for a change and still wants that developmental support provided by sidelying.

An exception would be if the sidelying position with specific  L or R side  down was prescribed post swallow study or post-ECMO or post-PDA ligation. Then the change should coincide with therapist guidance and, if indicated based on etiology,  a repeat instrumental assessment of swallowing physiology.

Problem-Solving: Ten Year Old with Cerebral Palsy

QUESTION:
I am a young clinician with a patient that has recently had a follow up swallow study that showed poorer results than original swallow study in absence of change in medical status.

Patient is male, 10 with CP. I’ve seen him for feeding and social/emotional communication around mealtimes due to intense frustration. Recently he got a swallow study that shows aspiration for thin and half nectar by straw and sippy cup due to volume. Nectar showed no a/p. Silent aspiration on 5/20 swallows. He eats all solids and had no a/p on previous and most recent MBSS.

Recommendation following swallow study was to use Thick It to nectar consistency. Also to use Vital Stim.

I’m looking for input on next steps in the home health setting. Is it worth it to discuss Frazier Free Water protocol with Mom? One consideration is he had a croup attack 2 months ago unexpectedly.

ANSWER: 

So glad you reached out. Lots of thoughts and questions as I read your post. Know that the questions and “thinking out loud’ are part of my clinical problem-solving, to sort out relevant considerations and complete differential as I go along. Just lots of questions and weighing of possibilities to start with. Usually, children with complex co-morbidities have multiple relevant components to their care to sort out.

“Poorer results than the original study” in this child’s situation, based on what we you have shared, could be the result of several possibilities.

Not sure how long ago the previous study was or the results, but the previous study may be part of the relevant picture: the analysis of that study might not have incorporated all the data or a bigger picture so the “results’ were precarious; the study was short or data was tenuous and conclusions were therefore tenuous; the etiology for the whatever adverse events were seen was not clear (or not made clear in the report) and perhaps, if it were,  would have given more information that might make sense now with newer data; physiology was not described, which would have provided more data than just what events of aspiration or laryngeal penetration were witnessed – remember Bonnie Martin Harris has told us that “aspiration or penetration is neither sufficient or necessary for a swallowing impairment”, so physiology becomes the key in our analysis; the study is always a moment in time and so we may not witness events that are indeed occurring during true meals.

A second relevant factor to consider is his neuromotor problems with a diagnosis of CP. While CP is not progressive, increasingly complex functional skills (including feeding) can sometimes look worse and become more challenging as time goes on, due to the demands on an already altered sensory-motor system to integrate for increasingly complex tasks over time.

A third relevant factor to consider as you reflect, is that children with CP often have related co-morbidities. We don’t know what his are from your description, but they can often include respiratory and GI, whose integrity may wax and wane, and therefore be fluid in their influence, pending for example the season of the year (e.g., winter can bring more respiratory challenges, spring can bring allergy-like factors in to play) , growth spurts, minimal changes in diet content that may seem at first glance as minimal, changes in activity. This can lead to subtle respiratory changes, subtle GI changes,  that in a dynamic system like the swallow, can influence function from moment to moment. The croup, which may have been part of an URI provoked by airway invasion from above or below, is worrisome.

Can you connect with the SLP who did the study and perhaps look at it together? It might suggest some added interventions that were or were not objectified, though likely were, such as: rate of intake, bolus size, cup utilized (there are so many and some work better for some children for safety), pacing, self-drinking versus fluids offered by caregivers, position and support/stability offered to optimize proximal and distal stability (seating device and support for the procedure can alter physiology in a good way or an adverse way).

Regarding a free water protocol, is he staying hydrated with the thickened liquids? Is he willing to drink them? Has his fluid intake gone down since thickening was started? Does he receive good oral care on a regular basis? What has his pulmonary health been like over time? can family carry it  over safely? Doesn’t sound indicated with what we know.

I hope this was helpful to get you thinking. It’s ok to live in the gray zone and not know these answers. Just thinking about them is part of the problem-solving process.

Problem-Solving: Two year old with Neuroblastoma and G-Tube

QUESTION:

I work with a child who is  two years old, and was diagnosed in October 2020 with neuroblastoma. She is fed through both a g-tube and by mouth minimally. Generally healthy. She completed chemotherapy at in April 2021. She began immunotherapy and will receive treatments one week per month (M,W,F).

Mom reports there was a never a concern for a true “swallow disorder” in regard to risk for pneumonia or ever a need for an instrumental swallow study. Mom reports that after her child was diagnosed with Neuroblastoma, the medical team considered an SLP to evaluate her swallowing due to an oral pocketing, lack of appetite and coughing concern; however, she was seen 1-2x by the inpatient SLP who deemed her “OK” and “fine” to eat, and “no need for instrumental”.

Per mom report, she was told that the feeding issue was behavioral/sensory, and that for nutritional / hydrational reasons, she received an NG tube, then a G-Tube was placed (end of November). Mom reports that she was told that her child can technically come off the G-Tube but since she wasn’t eating enough eating enough, it will remain placed.

Mom reports that now her child is being fed mostly through GTube and “not much” orally; reports approximately  2 spoons yogurt, OR 10 cheerios, OR dry cereal, nibble 1 bite of noodle, 1 bite of a freeze pop; mom reports that when she sees her siblings eat, she desires it, yet once given, she will throw it away.

I saw the child today; she ate 3 spoons of chocolate yogurt with no problem, 1/2 chip with functional oral skills and no overt issues. Mom then brought her favorite food: chickpeas (spicy flavor), the child ate about 10 pieces, then picked the last piece out of her mouth, gagged, burped, and proceeded to vomit a large amount of orange secretions. Given a sip of water, she began coughing.

When questioned, mom reports that this happens often with certain foods (“even the non-spicy chickpeas“), however they don’t always see it because she “hardly eats”. I recommended perhaps a GI consult and/or follow up with hospital SLP to consider instrumental exam.

 

ANSWER:

It is challenging when the infant’s/child’s history is provided solely by the parents. They may recall information incorrectly, forget critical details that would assist you, misinterpret what was said or what transpired, or perhaps have focused only on part of what they heard that might have been more readily understood or accepted at that time. On the inpatient side, especially after a critical diagnosis of neuroblastoma, the aftershock and the stages of grief set in for parents. They have told me it is like a fog sets in, it’s hard to remember what you heard, and it’s scary. During that time, information processing is very much affected by the stage of grieving they are in, the acuity of infant’s child’s medical situation, the early progress during inpatient stay and the multitude of consultants that come in and out of their daily lives, as they stay at the hospital, who touch them and their child each day. I see it first had as I am in the room with a family and an infant/child, a physician comes in to examine and update their differential and the talks with the family. Or the team does morning Rounds. It can be overwhelming for parents but intended to be so helpful. Everyone is typically thoughtful, and share a lot of crucial information, answer questions, listen. One parent might not be there due to being at work for example and gets the information second hand from a family member. After the physician leaves, the reprocessing often begins as the parent wonders aloud and then “digests” what actually transpired or what they heard through weary ears. Add this to the critical decisions made by the team and asked of the families when they are under emotional stress. I wonder sometimes how the families get up each day and come back so kind, so thoughtful, and so caring, yet completely drained so much of the time.  It is within this context that they then store and late recall for you on the community/OP side, the important information.

It is possible that the SLP did have concerns about swallowing safety, which would be likely given the diagnosis. The SLP may indeed have expressed this concern, and the team decided otherwise, which can happen.  The parent may have found the SLP’s concern about swallowing surprising and kindly with respect disregarded it. It is hard for parents with a sick child to think now even eating and drinking m might also be a problem and the child might “lose” that as well. Sounds like interim pleasure feeding trials might have been recommended or perhaps there was a plan to complete an instrumental assessment, and, for multiple reasons, it was cancelled and there was a plan to follow-up with OP study. Possibly mucositis r/t chemo was apart of the decision. So many possibilities. This is not to say that as inpatient SLPs we don’t look back and say “hmm, I wish I would have…”  or “I wonder if I had…”  That is a part of doing your best to minimize risk and improving one’s practice, thoughtfully reflecting on how we can do better. Without that SLPs input, we just don’t know what unfolded.

Perhaps ask Mother for a release of records for SLP services during IP stay and get her authorization to contact the SLP staff directly and speak with the SLP who cared for this child, to get that SLPs perspective and objective data. That will hopefully bridge the gap for Mother and for the child and for your planning your next steps.

Thanks for reaching out. We are all part of a big team that continues beyond the walls of the hospital, to support each other.

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

QUESTION:

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

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

ANSWER:

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

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

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

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

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

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

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

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

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

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

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

I hope this is helpful.

Catherine

 

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

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

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

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

 

Problem-Solving: Thickening Breastmilk Post Swallow Study

QUESTION

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

ANSWER:

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

But a simple answer may not be best.

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

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

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

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

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

I hope this is helpful.

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

Question:

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

Answer:

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

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

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

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

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

Hope this helps.

Catherine

Problem-Solving: SLP completing NGT feedings in NICU

QUESTION

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

ANSWER

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

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

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

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

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

I hope this is helpful.

Problem-Solving: Silent Deep Laryngeal Penetration

QUESTION:

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

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

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

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

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

DR. JAMES COYLE’S ANSWER:

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

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

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

 

CATHERINE’ S FOLLOW-UP COMMENT:

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

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

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

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

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