Ann writes:

<This is just my theory based on observation and some on the science of
how
our lymphatic system works.  Women with smaller breast are more likely to
exhibit more noticeable primary engorgement than women with very large
breast.  The smaller breast has less adipose tissue and the milk glands
are
closer to the surface, therefore there is less tissue space to expand
with
the filling from the lymphatic system.>

I do remember empirical advice I gave to small breasted moms in my
prenatal BrF class teaching days. I emphasized that they would be wise to
feed early and massage from the chest wall forward early and frequently,
before and between feedings, to help keep the milk moving forward so it
wouldn't crowd the back of the breast where more milk was being made.

That's long before I began to read extensively about the embryology and
anatomy of the breast. So I must have been in agreement with you then.
Now, I am seeing it in a different way.

One source describes the breast as a "cutaneous  envelope" (an envelope
of skin) containing different  kinds and amounts of tissue at different
times in life. It changes during each menstrual cycle. There is sometimes
edema in the connective during one part of the cycle, at least in younger
women. This may be causing the skin to expand slowly as the breast
develops.

I also read that that is one of the primary reasons for fat tissue in
breasts-to "hold the space", and maintain the architecture in the growing
gland, so that during pregnancy, the fat can be metabolically taken out
of the breast as the glandular tissue grows. In one study, at term, the
glandular tissue had grown to occupy >70% of the space, while the amount
of connective tissue (including fat cells) was reduced to <30%.

If so, then the woman with the small breast might be one who hasn't much
fatty tissue but has a "standard" amount of glandular tissue (in other
words, we're not talking here about glandular insufficiency).

I want to introduce a simple garden metaphor here that helped me to make
sense of the embryonic references I read:

Plant . . . . . . is to Soil as
Parenchyma is to Stroma.

Visualize the roots of a Plant growing down into the Soil.

Then visualize the ectodermal layer (the  parenchyma [the future
glandular tissue] of the breast) budding and sprouting "roots" downward
into the mesodermal layer (the stroma [future connective tissue,
including the lymphatic system] of the breast.

I was fascinated to read that during embryonic development, the mesoderm
is essential to developing the pathways through which the ectoderm then
grows. Without it, the parenchyma doesn't grow. (Good soil conditions
needed for healthy plants.)

Therefore my logic tells me that the mother with a "standard" amount of
glandular tissue would first have to have developed a "standard" amount
of connective (including lymphatic) tissue too.

If she experiences swelling within the glandular compartment, that might
expand her skin tightly if there had been little fat there in the first
place.

But once again, if we are talking about swelling within the glandular
tree, we're dealing with something that comes from delayed or inefficient
milk removal.

And that causes a "traffic jam" especially in the upper outer quadrant.
And this competes for available space that the lymph vessels need for
efficient drainage.

And if this mom had lots of IV fluid, plus perhaps pitocin, then she will
also get an abnormal amount of tissue fluid built up in the connective
tissue, making it difficult for even an "uncrowded" lymphatic pump to
remove rapidly enough.

So early, regular MER's, efficient latching and frequent efficient
suckling, with breast compression, or massage or fingertip expression if
needed to keep the milk moving, is the primary way to prevent back-up
inside the glandular tree. Efficient drainage of the glandular tree will
prevent physical blockage of the lymphatic pathways.

But steady entry of tissue fluid into the lymphatic pump might not be
able to keep up with rapid formation of excess tissue fluid, depending on
the amount of IV fluid given. (Tissue fluid enters from the circulatory
capillaries, and is not officially defined as "lymph" till it enters a
lymphatic vessel.)

The volume of IV fluids given has heretofore been a missing part of the
engorgement research equation. Likewise, the # of units of pitocin, which
can have antidiuretic properties.

It seems to me that there is enough evidence out there now to label these
as important variables. No articles on engorgement that I have yet seen
have taken these measured factors into consideration. I'd appreciate
learning about them if anyone can provide such references.

<Women with large breast describe
increase heaviness in their breast but I rarely find them with severe
engorgement compared to women with the smaller breast.>

Engorgement has been defined and described in a lot of different ways.
One way was to measure the actual "hardness" of the breast with an
electronic instrument. It sounds as if "hardness" is how you are
"measuring" comparative engorgement. I would think that one where the
skin was stretched to it's limit would also feel more painful, a way that
other engorgement research measured degrees of engorgement.

So I can see how a larger breast might still have enough space once the
fat cushion was reduced, so that the skin might not be as stretched,
might not feel as hard, or as painful, even with the same degree of
fullness of the glandular tree and the same conditions effecting
formation and removal of tissue fluid through the lymphatic pump.

<Where I find this dilemma more challenging is in the areola.  In the
smaller
breast the areola gets much firmer during engorgement than the larger
breast
and therefore babies refusing to latch on day 4 when they were doing fine
in
the hospital.>

We are all familiar with watching balloons expand, and I think it
provides a good model here. When you blow up a small balloon, the tip
disappears more quickly than when you blow up a larger balloon with the
same amount of air. And the small balloon feels firmer, because it has
less surface area, and therefore is stretched more tightly, to contain
the same volume of air.

I believe excess subareolar tissue resistance is an unidentified piece in
the puzzle of poor latch, ineffective suckling and nipple pain and
damage. And although I'll agree it's probably seen more often in women
with smaller size breasts, I'm not certain the larger breasted mom
escapes it.

What you have described as the firmness of the areola interfering with
latching has been the basis for my thinking in developing the concept of
Reverse Pressure Softening. See http://health-e-learning.com and click on
"Research Articles".

Jean
****************
K. Jean Cotterman RNC, RLC, IBCLC
Dayton, OH

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