Latest research on the effects of oral feeding while on nasal continuous positive airway pressure (NCPAP) in preterm infants

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 Perinatology, 1-7.

Louisa Ferrara, PhD SLP contributes to the science that underpins our growing understanding of the potential risks of asking preterm infants to PO feed while they continue to require NCPAP. This information will inform your practice in the NICU and can promote needed discussion among members of the NICU interdisciplinary team

Objective To determine whether delaying oral feeding until coming off NCPAP will alter feeding and respiratory-related morbidities in preterm infants.

Design In this retrospective pre–post analysis, outcomes were compared in two preterm infant groups (≤32 weeks gestation).

Infants in Group 1 were orally fed while on NCPAP, while infants in Group 2 were only allowed oral feedings after ceasing NCPAP.

Results Although infants in Group 2 started feeds at a later postmenstrual age (PMA), they reached full oral feeding at a similar PMA compared with Group 1. Interestingly, there was a positive correlation between the duration of oral feeding while on NCPAP and the time spent on respiratory support in Group 1.

Conclusions:  Delayed oral feeding until ceasing NCPAP did not contribute to feeding-related morbidities. We recommend caution when initiating oral feedings in preterm infants on NCPAP without evaluating the safety of the infants and their readiness for oral feedings.

Pursuing Certification in Lactation

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

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

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

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

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

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

Problem-Solving Bradycardia during PO in the NICU

Question:

We currently have a former 33 week twin, now 36 and 4 weeks who frequently demonstrates bradycardia events but only during feeding attempts. He does not drop is oxygen saturation at all, in fact this almost always remains at 100% during feeding. His drop in heart rate is usually brief but this is usually after being stimulated. He wakes up consistently for feeding, shows appropriate feeding readiness cues, has a very strong non nutritive suck pattern. With bottle feeding attempts he demonstrates a very poor suck/swallow/breath sequence. He was initially on the ultra preemie nipple to slow the flow down to assist with coordination, however would demonstrate a very fast rate of suck, inefficient with fluid expression with suspected oral pooling in the posterior oral cavity prior to swallow. We have trialed a preemie nipple but without much change in his pattern with the goal of trying to achieve a more functional suck to swallow ratio. I do feel his swallow response is delayed post suck and inconsistent throughout the feed depending on alertness. Could these frequent bradycardia events be a vagal response? As a result of aspiration? Any positioning or flow rate recommendations to trial instead? You can very much tell when he is going to drop his heart rate during a feeding, and usually with re-positioning, taking a break from the feeding it can be prevented but I’m still curious as to a possible etiology for this. He is still currently on caffeine due to these frequent events. Any insight appreciated.

Catherine’s Answer

This is a challenging clinical presentation to problem-solve but not an uncommon one in the NICU. Can you tell us any more about the infant’s history and co-morbidities (especially respiratory, neurologic, GI, postural/sensory-motor?) is he otherwise progressing as one would expect of a former 33 weeker now 36+ weeks PMA?

Bradycardia events during PO feeding can occur at 36 weeks PMA but such are not typical of preemies at that age and are unlikely therefore to be “a variant” of prematurity itself. Some bradycardic events during PO occur without co-occurring desaturation, especially if the bradycardic events are not prolonged. However, the provoking of a bradycardia when the infant PO feeds is worrisome none the less. Bradycardia in NICU infants during PO was correlated with aspiration in a study/paper by Neina Ferguson in 2015.

When I think about a differential as to about what co-morbidities might provoke such episodes at 36+ weeks, what comes to mind includes : GI (e.g., EER/LPR), respiratory (swallow-breathe incoordination leading to uncoupling of the swallow -breathe interface secondary to increased WOB, intermittent tachypnea). Both may present a pathway to airway invasion. In addition, alterations in neural integrity (which can occur in a former 33 weeker but are less likely to be the sources of provocation than the other two possibilities I mentioned). There can also be caregiver artifact (i.e., not recognizing and/or responding to infant’s physiological communication and/or swallowing behaviors from moment to moment , to contingently titrate interventions to avert decompensation; using a flow rate that is too fast, well-intentioned prodding). The last possibility, caregiver artifact, seems unlikely given that he is having these events with you, not only with, for example, parents or staff. But some added interventions might help; more on that later.

Your clinical description suggests a prolonged sucking pattern, likely in the setting of increased WOB and intermittent tachypnea. An increase in WOB may be [resent at baseline or can be recruited (or exacerbated) by a strong continuous sucking effort, without timely and sufficient breaths. This can lead to the need for an urgent breath, even with flow rate control via Dr. Brown’s premie or ultrapremie nipples. Bolus sizes beyond the infant’s capacity can then perhaps “overwhelm” the required dynamic adjustments of his airway that need to surround the swallow. This may lead to a clinical impression of a delay in onset of post-swallow breath (due to the infant’s attempt to prolonged airway closure as a means to protect the airway). Along the swallow pathway, the infant may attempt adaptations that, unfortunately, create resulting maladaptations that lead to further risk for laryngeal penetration and/or aspiration.

In my clinical experience, bradycardia during PO at 36 weeks PMA, even with interventions in place, is most often correlated with airway invasion. A vagal response can indeed result in bradycardia but is often seen as a maturational variant, again unlikely at 36 weeks PMA. Polyvagal Theory, which is quite complex, postulates and describes the fragile nature of CN X function related to prematurity.

When fluid approaches the airway of a preterm infant, there is a reflex that is supposed to be elicited to close the airway; however, its timeliness, consistency of provocation and effectiveness are not well understood. Caffeine prescribed to stimulate HR as you describe can have the unintended sequelae of increasing EER//LPR, so EER/LPR could still be part of the differential too.

Without knowing any more about the infant’s history and co-morbidities, I would suggest you continue to contingently rest the infant, use controlled flow rate to limit bolus size, and, if you have not trialed it yet, use elongated swaddled sidelying (to optimize tidal volume and respiratory reserves). Then incorporate contingent co-regulated pacing based on the infants communication and swallowing behaviors.

If, with these interventions, you cannot avert the events described, I would instrumentally assess swallowing physiology to help elucidate the etiology(ies) for the events, and the effect of further titrated interventions (frequency of pacing, flow rate). Unfortunately, some of our preterms who have adverse overt events during PO feeding are also observed to silently invade their airway under fluoroscopy.

I hope this is helpful.

Problem-Solving: Fluoro Time for Neonates

Question:

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

Catherine’s Answer:

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

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

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

Problem-Solving: Respiratory rates in neonates

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

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

Catherine’s answer:

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

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

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

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

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

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

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

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

Problem-Solving: Vocal Cord Paralysis and Sidelying

Question:

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

Answer:

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

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

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

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

2020 Catherine Shaker Seminars: New Offering!

As the New Year approaches, I look forward to travelling across the US, meeting colleagues with a similar passion for “all things feeding and swallowing”. While I love teaching, I also love learning from the therapists I meet and making lasting friendships as well. We each have so much to share and I never stop learning .

I have added a new seminar for 2020: Advanced Infant/Pediatric Dysphagia: Problem-Solving Complex Patients and Practice Challenges Two days of problem-solving designed just for you and your patients, NICU through school aged. We’ll discuss complex diagnoses, hot topics in dysphagia (for example: thickening, NMES, oral-motor “exercises”) and current practice issues such a team communication, managing challenging clinical situations, and navigating therapist-physician relationships in the intensive care unit. I look forward to learning along with you

Pediatric Swallowing and Feeding: The Essentials – 13 hours contact hours – 2 days Pediatric

Videofluoroscopic Swallow Studies: From Physiology to Analysis – 6.5 contact hours – 1 day

NICU Swallowing and Feeding: In the Nursery and After Discharge – 13.5 contact hours – 2 days

The Early Feeding Skills Assessment Tool: A Guide to Cue-Based Feeding in the NICU – 13 contact hours – 2 days

Advanced Infant/Pediatric Dysphagia: Problem-Solving Complex Patients and Practice Challenges – 13 contact hours – 2 days

Locations

Nashville – May

Houston – June

Orange County CA – July

Chicago area – August

Phoenix – September

Greenwich CT – October

Watch for details soon on my website or sign up for my blog and you will receive automatic notice when my seminar schedule and brochure are posted in January.

Wishing you abundant blessings in the New Year ahead. I hope our paths cross in 2020!

Catherine

Problem-Solving: Sensory Normalization with Rubinstein-Taybi Syndrome

Question:

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

Answer:

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

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

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

Problem-Solving: Former Preterm with Beckwith Wiedemann Syndrome

Question:

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

Answer:

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

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

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

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

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

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

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

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

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

Problem-Solving: Late Preterm with Sequelae from Mandibular Hypoplasia

Question:

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

Answer:

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

Problem-Solving: Initiating PO Feeding in the NICU

Question:

My colleagues and I have been discussing the age at which to start bottle feedings. I realize it will depend on the child’s development, their history, their stress level, and rooting behavior. But in writing a policy for the NICU for cue Based Feeding I was hoping for a starting age. We’ve said 33 weeks or greater. I have a NICU manager who is pushing for 32 weeks, and a neonatologist who wants to stay away from a defining age. Currently we have “CBF to begin 33 weeks or later. Any infant younger than 33 weeks to be assessed by speech therapist first.” But that last statement has yet to be approved. And I was hoping to have literature to back the age. Any feedback is much appreciated.

Answer:

The question about when NICU infants initiate PO feeding is of course multi-factorial, so PMA (post-menstrual age) is just one factor. Unfortunately, while it puts us in “the ballpark”, it has little value in and of itself. The PMA has significance, I like to say, in the context of the infant’s co-morbidities and history. Considering only PMA without regard for co-morbidities and history can lead to first PO feedings that are physiologically stressful, adversely affect neuroprotection and set the stage for feeding early onset refusals as a result, as you know. Some infants at a particular age, for example, 37 weeks PMA may not be ready/appropriate to PO, often due to the sequalae from their co-morbidities and history.

As I teach across the US regarding NICU feeding/swallowing practice, the earliest I have heard PO feeding being initiated is 31 weeks PMA. This has typically been a healthy preterm stable on unassisted RA and with a clean history; but even then, readiness of requisite subsystems, such as postural/head/neck control and state modulation, may not be available for that infant, and the suck-swallow-breathe interface is likely quite precarious. Asking the infant to feed 9 weeks prior to his due date would be worrisome. The push to “get infants out” and the desire to “get infants home” has created undue pressure on the infants, staff and in-turn on families to “get it in”.

Perhaps that is why the neonatologist is suggesting avoiding a defining age and is looking instead, hopefully, at a more global assessment of the infant. Alternatively, he/she may be leaving the door open to push harder unfortunately . Carrie Anne’s reference should be helpful but unfortunately Dr. Pickler often has a focus on “practicing” PO as a benefit and the pathway to good outcomes. While some in the NICU think “practice makes perfect” when it comes to feeding, unfortunately, when feeding attempts are ill-timed or are not truly supportive, then “practice”  only makes “permanent”   the emotional overlay and activation of the HP axis/cortisol release associated with physiologic stress in preterms, that likely co-occurs with trying to feed and struggle. Contrast that with an infant-guided feeding approach , truly cue-based PO feeding, that focuses on the experience and neuroprotection, versus intake.

Individualized readiness using multiple factors, one of those factors being PMA, is ideal an most supportive of neuroprotection. I am not aware of any research that has specifically determined “the age” to start, as so many variables indeed must be taken into account as I referenced above. That would be a hard study to do and do well. My thought is that 33-34 weeks PMA is likely most typical across the US based on feedback I solicit in every city I teach. If you can help to build criteria that encompass not only age (PMA), but a more comprehensive look at the infant, then perhaps there will be room purposefully built in to individualize and assess that unique infant’s readiness in the setting of his co-morbidities and history.

Research Corner and Commentary about Article in the ASHA Leader on Thickening in the NICU

This is an excellent article just published by our colleagues at Boston Childrens and will inform your practice.

Duncan DR, Larson K, Rosen RL(2019) Clinical aspects of thickeners for pediatric gastroesophageal reflux and oropharyngeal dysphagia.
Current gastroenterology reports.  https://doi.org/10.1007/s11894-019-0697-2

Abstract
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. Recent Findings: Thickeners are effective in decreasing regurgitation and improving swallowing mechanics and can often be used
empirically for the treatment of infants and young children. Adverse effects have been reported, but with careful consideration of
appropriate thickener types, desired thickening consistency, and follow-up in collaboration with feeding specialists, most patients have symptomatic improvements. Summary Thickeners are typically well tolerated and with few side effects, but close follow-up is needed to make sure patients tolerate thickeners and have adequate symptom improvement.

On a related note, I feel compelled to address a recent article in The ASHA Leader “From My Perspective: Overuse of Thickeners in the NICU.”

The article, I believe, while certainly written with the best of intentions, has the potential to set back the progress SLPs have made delineating a critical well-respected evidence-based role in the NICU and, left unaddressed, could do harm.

I am concerned that  SLPs (both adult and pediatric)  who are unfamiliar with the work of NICU SLPs may, after reading the above mentioned article in The ASHA Leader, have an inaccurate the impression about our practice. The article appears to make assumptions, and appears to question the clinical reasoning that underpins decisions made every day, with deliberate consideration for short and long-term implications and for best practice.

Many of the assumptions made by the author  are not consistent with both my practice in large level IV  NICUs for the last 35 years, nor the practice of most other NICU SLPs I have met as I teach across the US about NICU intervention. While there may indeed be variability in the knowledge and practice of some NICU providers (Madhoun, et al 2015),  the AAP recommends caution with thickeners in preterm infants, and this is typically the overriding consideration for all interventions prescribed in the NICU. First, do no harm. 

The author’s statement that “thickeners are a long-term solution” is not consistent with typical NICU practice. Thickeners are used only as the last resort in the NICU (Gosa, 2015) —- after trialing changing feeding position, slowing nipple flow rate, utilizing contingent  co-regulated pacing to support the swallow-breathe interface and assure timely and sufficient breaths.  Even then, thickening may not be the safest solution for a specific  infant and can  present untoward sequelae ( higher risk to aspirate after the swallow, concerns of digestive immaturity, malabsorption, NEC, etc.) Most NICUs rarely use thickeners today to the extent that they were used in the past, and if thickeners are, it is viewed as short term. In dialogue with the medical team, there is typically careful interdisciplinary deliberation of the risk benefit ratio. If indicated, there is typically the contingent use of interventions to minimize the risk, and support both oral-motor learning and motor learning, and avoid maladaptations that may result.

Each NICU infant’s  developmental progression, respiratory, GI and neuro history and co-morbidities must be considered, as well as the nature of the pathophysiology objectified in radiology.  When the author states that “failing a swallow study” is a reason to thicken, it suggests the author considers a swallow study as a “pass-fail procedure”.  Rather than a pass-fail procedure, an instrumental assessment is viewed with the NICU population, as an analysis of swallowing physiology, its alteration or impairment, and its implications for that unique infant in the setting of his unique presentation/data set.  Like with other populations for whom SLPs provide services, a neonate does not need to penetrate or aspirate to have a swallowing impairment that may lead to airway invasion. As a result, the level of analysis that is required, and the essential caution as to prescribed interventions, is well understood by those of us working with this high risk fragile population in the NICU. Thickening may be contraindicated based on data obtained in radiology.

The author asks  “What if the baby can’t suck?” and then states that “all babies have a suck reflex”. Unfortunately, this is inaccurate. It is not uncommon that a sick newborn or some preterm infants with significant neurologic co-morbidities may not have a sucking reflex, or the suck lacks the integrity to feed orally. If  indeed this is the clinical presentation, thickeners would be contraindicated. Our  interventions for motor learning would go in a completely different direction, both in the NICU and after discharge.

In addition, the assumptions about the interventions described in the article for use with post NICU infants (e.g., bottle feeding thin liquid  to avoid maladaptive feeding patterns, use of glycerin swabs, ice chips, and anterior controlled placement of thin water) are worrisome and may mislead the reader as to the interventions most typically indicated for an infant just discharged from a neonatal intensive care unit. The infant post-NICU is often still quite immature overall, and interventions such as those suggested may both present undue risk to the airway and be poorly tolerated from a sensory and GI perspective. Indeed, safety of progressing the diet to thin liquids, if previously contraindicated, would best be considered for the NICU graduate in the setting of objective data regarding physiology in radiology. Many NICU graduates continue to have medical issues post discharge that can make airway invasion a compelling risk to both their pulmonary and overall health. 


Cichero, J A  et al (2013). Thickened milk for the management of feeding and swallowing issues in infants: a call for interdisciplinary professional guidelines. Journal of Human Lactation, 29(2), 132-135.

Duncan DR, Larson K, Davidson K, May K, Rahbar R, Rosen RL.(2019) Feeding interventions are associated with improved outcomes in
children with laryngeal penetration. J Pediatr Gastroenterol Nutr. 68(2):218–224.

Goldfield, EC  et al (2013) Preterm infant swallowing of thin and nectar-thick liquids: changes in lingual-palatal coordination and relation to bolus transit. Dysphagia 28, 234e244.

Gosa, MM & Corkins, M R(2015). Necrotizing enterocolitis and the use of thickened liquids for infants with dysphagia. Perspectives on Swallowing and Swallowing Disorders (Dysphagia), 24(2), 44-49.

Madhoun, LL et al (2015). Feed-thickening practices in NICUs in the current era: Variability in prescription and implementation patterns. Journal of Neonatal Nursing, 21(6), 255-262.

I appreciate the opportunity to share the perspective of an NICU SLP and hope this has been helpful.