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Subject:
From:
Katharine West <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Sun, 27 Jan 2002 22:51:01 -0800
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> The mothers commenced breastfeeding as
soon as the infants did not need ventilator/CPAP, from 26 postmenstrual
weeks (corresponding to 24 weeks PCA). Irrespective of maturational level on
the first day with breastfeeding, all infants demonstrated rooting, latched
on, and sucked (there were a few exceptions, infants at 33-35 weeks PMA
(31-32 PCA).

Interesting post. May I add to it? I was at the California March of Dimes
conference held just these past 3 days in Long Beach and heard an excellent
presentation on fetal/neonatal neurology by Harvey B. Sarnat, MD, Professor
of Pediatric Neurology and Neuropathology at UCLA School of Medicine. I
learned much from his presentation "Disorders of the Brainstem in the Human
Fetus and Neonate" in which he provided, amongst other things, reasons for
why we can find premies who can breastfeed early, as written in the above
post. I like explanations for things observed that challenge the status quo,
like, just why is it that some 27 weekers feed and yet many NICUs won't even
attempt oral feeds until 32-33 weeks gestational age? Turns out there is
support for both scenarios.

From Dr. Sarnat's presentation: "Sucking and swallowing are among the
tactile reflexes [including several others which he discussed], which are
basic brainstem reflexes and part of the corticospinal tract. In the fetus
and the newborn, the function of the corticospinal tract ... includes the
reinforcement of the tactile reflexes. Tactile reflexes are fundamentally
mediated by segmental circuits in the brainstem and spinal cord to be
functional. ... These reflexes become impaired if corticospinal function
previously was intact and the infant has suffered an acute or subacute
removal of normal corticospinal reinforcement. ...Impairment of CST function
at the cortical level is non-specific and may be due to ischemic/hypoxic
encephalopathy at birth, congenital infections, neonatal meningitis,
hydrocephalus, subarachnoid hemorrhage from traumatic delivery, impairment
from systemic metabolic diseases, neurotoxins or drugs, or many other
causes. The clinical signs of CST impairment, as isolated findings, do not
imply prognosis. The impaired CST may be reversible with neuronal recovery
..."

In his review of neurological findings of neonatal dysphagia, he discussed
the swallowing mechanism being "impaired by ischemia or infarct in the
region of the tegmentum of the medulla oblongata due to hypotension.
Neonates thus affected may be unable to swallow or have poorly coordinated
swallowing and aspirate easily."

Basically, what I understood, was that as long as the baby does not have
impaired corticospinal tract (CST) function, the tactile reflexes (normal
and early appearing brainstem reflexes that they are) will be present and
feeding attempts will be successful even at young gestational ages as
described above. But look at the list of events that can cause impairment -
it is a wonder any premature ever feeds in the NICU!

It may be found that prolonged ventilatory support (defined differently by
different researchers but probably something around 6 days or more) and
possibly several other currently acceptable therapies in the NICU may
eventually be determined to cause impairment to the tactile reflexes (by
reason of tiny infarcts). Perhaps we'll find (like giving too much oxygen in
the 60s - we kept the baby alive but caused blindness) many premies today
are not able to manage feeding until 32-33 weeks gestation because our
current interventions have actually caused temporary impairment of the CST.
Maybe due to "neuronal recovery" or even ongoing neurological maturation, 33
weeks is when we see the majority of infants demonstrating their tactile
reflexes of sucking and swallowing finally. It just so happens that
sequential myelination of the CST pathways begins about that time and
perhaps helps recover this critical survival skill (medial subcorticospinal
pathway myelination is complete first at 33 weeks, lateral next at 40 weeks,
followed by the CST itself even later). (Of course, this begs for breastmilk
feeds, because only breastmilk provides the type of lipid that accelerates
myelination in the human nervous system.)

The take-away point to all this, is this: knowing the health history counts
for much and care should be individualized. Knowing that these tactile
reflexes will be present in the 23 weeker is good news for early feeding
attempts but only if the CST is not impaired by reasons of infection, brain
infarct, prolonged ventilation, etc. Also, the CST can recover over time.
Since even MRIs are not going to show the detail needed to see that
recovery, we have to watch for the return of these tactile reflexes in
babies so affected and begin oral feeds when we see sucking and rooting.

I would argue that the 27 weeker who has had a great adaptation to
extrauterine life (without prolonged ventilation or infection or many drugs)
should be allowed to attempt oral feeds and be supported to succeed, yes
even that young if capable. By the same token, a baby who perhaps was born
at 32 weeks but with maternal infection as well as hypoxia during delivery
and ventilatory support for more than 6 days due to meconium aspiration
might just have an impaired CST with an equally impaired suck-swallow until
neuronal recovery can take place - that's the baby who may still be
dysphagic at 35 weeks - but he'll outgrow it (we hope).

Anyway, that's how I understood Dr. Sarnat's talk and why I found it
explained how both scenarios (the 27 weeker who can and the 32 weeker who
cannot manage oral feeds) could be true. I hope I did Dr. Sarnat's
presentation justice - he of course covered much more territory and detail.

Katharine West, MPH, MSN, RN
Sherman Oaks, CA

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