Helen writes:

<I advised mom to soften breasts before feeding by using manual expressing
or pumping a small amount, and to feed baby more frequently so that
feedings are calmer.
 I also offered some suggestions to try to elicit a MER - warm compresses,
gentle massage, thoughts/images of her beautiful newborn.  She responed " I
'm not supposed to watch the pump the whole time?"
Baby seemed fussy again.  We tried to latch the baby to the breast again
without success, then tried the bottle, she was not interested either.
I am going back tomorrow and will teach reverse pressure softening and try
to convince mom to try spoon feeding.>


I want to reinforce that my experience has shown that teaching RPS as the very first intervention,before any swelling is even noticed, and encouraging it to be used consistently before every feeding and before and during every attempt to pump will save much of the trouble described here. 


To begin with, I have never yet seen RPS, when held for at least 1-2 minutes, fail to trigger an MER within 1-3 minutes or so. It stimulates the nerves directly under the skin of the areola as they wend their their way from all around the breast to the underside of the nipple to enter its center from there, and sends the neurological arc of the MER quickly to the pituitary. It then only remains for the oxytocin released to navigate its way through the circulation and the interstitial fluid to reach the myoepithelial cells to make them contract. The mom may not necessarily be conscious of any sensation when it happens, but RPS "frees" the ducts in the subareolar area by pushing the Pre-L-2 edema upward away from them so they are temporarily "un-crowded", whereupon there will be a noticeable change at the moment the MER starts changing the milk flow.
  

First clue-moms with C/S/anesthetics: Intravenous fluids, and check the history to see if more than 2 bags were given in a 24 hour period. (Mom probably can't remember exactly). Pre-L2 edema is often one of the first results of receiving >2000 cc./in any one 24 hours, especially if hours of pitocin drip is given either for induction, augmentation or hours of third stage maagement, since the pitocin molecule is capable of occupying the binding site for ADH in the kidney. (Nature is a smart old gal. Pulsatile oxytocin released naturally at MER tells the kidneys "Don't be in a hurry just yet to get rid of too much fluid. If this kiddo removes a good amount of milk, at least one of those breasts is gonna have to pull some H20 out of the "interstitial pantry" to hurry up and make more milk pretty fast during the next hour or so. If little or none of the milk gets removed after this MER, during the "rest" between natural pulsatile release, you can do your thing with that H20 . . . .") But among other things IV pitocin drip is not pulsatile.


Pre-L-2 edema often makes it difficult or impossibe to hand express. RPS displaces the edema temporarily to facilitate HE.


Pre-L-2 edema is outside the boundaries of ducts and/or blood vessels and lymphatic vessels. It pushes its way forward like a swamp after a flood. It is trying to neutralize the negative pressure of vacuum (which does not actually pull: other forces push) This is all the more likely to happen if the breast is C-cup or beyond due to gravity leading the weight of the edema to the lower part of the breast. This crowds the ducts, plus buries them under further edema so that very little of their pressing against the flange can effect them and exert hydraulic pressure on the milk in the subareolar ducts, so at this stage, vacuum often makes things more complicated rather than improving the flow of the milk.


Got wound up, had to post, but I need to stop and go to WIC at this moment. Anyone wishing to recieve a further attachment on Pitting Edema, e-mail me privately.


K. Jean Cotterman RNC-E, IBCLC
WIC Volunteer LC  Dayton OH

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