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.
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.