Question

I have a 9 year old girl on my caseload with an open mouth posture  She presents with normal cognitive abilities and is compliant towards sustaining a closed mouth posture .  However, the day is long and memory is short.  Therefore, I would like to provide her with strategies to remind herself during the day in order to maintain this position    Any suggestions are welcome

 

Answer

The biggest question for me is why, what else could be going on? I would look to solve the etiology before trialing treatments that may not be applicable given what the etiology actually s.

Oral-motor problems can exist in and of themselves but, in my experience,  they are part of a bigger picture that must be considered. Considering the potential impact of the postural mechanism, the sensory system and the feeding/swallowing pathway in its entirety, often helps to solve a clinical puzzle such as the one you pose.

Some questions I have to help problem-solve:

Does she and/or do  parents report this is new onset behavior? Was it observed in infancy? Is it longstanding? If not, what prompted the referral  at age 9?

Are there any past co-morbidities from which  this may be part of the sequelae? These may be from birth, or alterations along her developmental trajectory that may not be so obvious now. You will need to ask parents and look beyond the obvious. If there are past co-morbidities, for example if there is even mild postural hypotonia in infancy, the sequelae we would see at 9 may be more subtle but affect function as you report.

Does she appear otherwise grossly normally developing in her sensory, gross-motor, and fine-motor and perceptual motor skills? I ask because I have learned from some fabulous OTs that sensory integration skills that underlie all these systems and can lead to what can look like “isolated” aberrations but are not.

An open mouth posture may be compensatory/purposeful (i.e., it is being used for a purpose, and does not reflect  a “mandibular” or muscle problem in and of itself) OR  it may be pathologic (related to alteration in the muscle synergies that stabilize and provide the dynamic synergies for suprahyoid/infrahyoid function)  OR it could be purely habitual which is very unlikely, given what you have told us.

Is her breathing quiet or is there some audible turbulence in airflow whether on inhalation or exhalation, suggestive of potential obstruction to/alteration in nasal airflow?

When she establishes a closed mouth posture, does that maneuver provoke any changes in her work of breathing (i.e., breathing effort) or her RR?

Tell us about her oral-motor skills, both for speech/conversation and during eating/drinking. Do you see the full ROM and strength and coordination that underpin both those functional skills? Is her voice or swallow altered in ways that are suggestive of tonsillar or adenoidal hypertrophy?

What about her saliva swallows? If the open mouth posture is predominant, she would likely have anterior loss of saliva bolus. Does she actually establish an anterior seal at the moment of the swallow and is it effective? Does she have other sensory challenges that may not be readily apparent but might be a part of the differential.

I would request an ENT consult to assure integrity of the nasopharyngeal airway, rule out any other structural etiologies and assure patent nasal airway, while you are sorting out the pieces that are or are not in your clinical differential.

Its ok to be in the “gray” zone for a while and not have the answers right away,  and take time for reflective thinking to sort this out. I suspect it is not that simple, but more comple.x

QUESTION

Can you recommend a chair model to use for pediatric infant and child video swallow studies and teen swallow studies?

ANSWER

Some general considerations:

If you need to use a C-arm (versus standard x-ray table), it may limit ease of access for certain seating devices and may limit establishing required view (i.e. child’s travel chair/wheel chair may seat the child too low to allow the desired view/image).

If the standard x-ray table is used, travel chair may be too wide with a tray in place to fit; yet if we take the tray off so chair fits in the narrow space, we change the postural stability typically available for PO feeding, and then may create an artifact in the data set.

Some very helpful seating devices go off the market randomly and we are left searching for a replacement

Need to consider if plan is to objectify typical position or optimal.

So problem-solving always a key, as is thinking outside the box.

I really like the MAMA Chair — Multiple Articulation, Multiple Adaptation chair, as Joan mentioned above. Flexible for different ages and levels of postural control and optional supports, hip-pelvic angles, has a footplate for optimal stability, which sounds not so important, but it is. Ever go out for a drink and end up on a bar stool with no rungs? You don’t stay long! Foot stability transfers throughout the entire postural mechanism and can affect swallowing/feeding skill. Just wish it had a tray to provide upper body stability via weightbearing, as that really can make a difference for some children too. We usually create something with very firm towel rolls to simulate a weight bearing surface. It is well worth the investment.

Some options for infants: Tumbleforms infant seat, infant seat/car seat, MAMA chair, swaddled sidelying on a wedge. Tumbleforms may create too rounded of a hip-pelvic angle if there is any postural instability, and that can adversely affect oral-motor swallowing function or generate maladaptive patterns.

Some options for toddlers: Secure larger Tumbleforms seat on Hausted chair( same caveat above applies), MAMA Chair, Special Tomato MPS seat , Hi Low Tomato Seat

Some options for children: same as above but may also be able to sit in regular chair (pending sensory-motor skills),  Rifton toileting chair with a cushion insert, Transmotion chair, Snug Seat Tiger High Low chair.

I hope this is helpful.

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.

Magyar, Hannah R.; Metzger, Laura D.; and Schrage, Ariel N., “Systematic Review: The Effects of Nonpharmacological and Pharmacological Measures in Neonates with Neonatal Abstinence Syndrome” (2019). Williams Honors College, Honors Research Projects. 889. https://ideaexchange.uakron.edu/honors_research_projects/889

Abstract

With the increasing incidence of drug addiction among pregnant women, neonatal abstinence syndrome (NAS) has become a significant problem in the United States and has led to increased hospital costs, longer lengths of stay, and more serious health problems in neonates. This systematic review will explore the evidence about outcome differences for neonates with NAS that receive breastfeeding, rooming-in, and acupuncture in addition to pharmacological agents when compared to infants only receiving pharmacological agents. Twenty-one articles, retrieved from the databases PubMed and CINAHL and published between the years 2000-2017, were described in an integrated review, analyzed with critical appraisal, and synthesized for this systematic review. In general, researchers have found that breastfeeding, rooming-in, and acupuncture have positive effects of decreasing the need for pharmacological treatment, NAS symptoms, hospital costs, and length of hospital stay for infants with NAS when used in conjunction with pharmacologic agents.