I want to add my $.02 to this stimulating discussion.

(I'm not convinced that I'm ready to jump all the way on the cabbage
bandwagon yet. I still feel uncomfortable with the many generalities and
the few specifics I continue to hear that seem to defy logic. My mom said
I was already asking "Why" about everything when I was 5 years old.)

Surgeons use the general term "engorgement" to describe the hormonal
swelling in the non-pregnant, non-lactating breast which occurs monthly
as a result of the menstrual cycle.

The breast seems designed to weather a certain amount of "waxing" and
"waning" of  circulatory, interstitial and lymphatic fluids as part of
its normal non-pregnant physiology.

When we as LC's use the term "engorgement",  we're usually speaking about
a postpartum condition in which there are at least 3 types of excess
fluid in 3 or more types of compartments, all of which are constructed
differently from each other and work in different ways.

1) a necessarily increased amount of blood within the blood vessels,
which travels in a circular fashion, into, through, then out of the
breast area.

2) a gradually increasing amount of milk within the ducts, which needs to
travel forward, down and out of the breast.

3) extracellular fluid between cells (interstitial), which eventually
needs to travel the opposite direction -into lymphatic capillaries and
thence upward and inward toward the chest wall and armpit.

When interstitial fluid increases beyond 30% of normal, it is then
referred to as edema, and has become visible to the naked eye.

Perhaps our terminology needs a little fine tuning and specificity.
(Perhaps we could somehow incorporate the term "3rd space" which other
HCP's already use.)

Postpartum engorgement resembles a "traffic jam" in the breasts. Maybe we
need to think a little like traffic cops. Concentrate on getting certain
lanes moving first, then give the others a chance, etc., then back to the
previous lanes.

There is no exact telling what percent of breast size increase is due to
each category of fluid. Indeed, the percentage probably differs from
mother to mother, day to day, hour to hour, and feeding to feeding.

But I think it's worth assessing whether milk or tissue fluid constitutes
the greater part of the mother's current swelling before deciding on a
"one treatment fits all, the same every postpartum day" intervention.

Unrelieved pressure in any single compartment would seem to increase
overall pressure in the breast, and raise the risk of milk suppression.

Any kind of massage can help stimulate MER, but forward directed
compressive massage helps to physically propel milk forward. One would
expect the milk component to begin to increase more and more beyond day
2-3.

If a particular mom's swelling consists more of enlarged blood vessels
and milk, perhaps that is why some cases respond well to forward massage
under a warm shower.

If we stimulate MER and move milk out of contact with the alveolar
surface and through the ducts, by my logic, we are reducing the chance of
suppressing milk production.

However, after that is accomplished, maybe we ought to give more thought
to inward directed massage [like the flats of the fingers when doing a
monthly breast exam].

Perhaps the elastic netting Rachel describes may be of more help to that
part of the swelling which is extracellular (intersitial) fluid. IME,
this component is often a larger part of the engorgement on day 4-5-6+
especially if a mom has had IV fluid, pitocin induction, etc.)

(Rachel, tell us-just how tight is the elastic-anything like our elastic
bandages? As firm as a firm bra? Or could it be the "Hawthorne effect"
that someone cares enough to take the time to gently and personally do
something non-mechanical to the whole of the breast area?)

I ran across an interesting factoid about the application of cold in my
trusty 23-year old Guyton "Basic Human Physiology" text: "When cold is
applied directly to the skin, the skin (blood) vessels constrict more and
more down to a temperature of about 15 degrees C. (which I calculate to
be about 59 degrees F.), at which point they reach their maximum degree
of constriction. . . . . . At temperatures below 15 degrees C., the
vessels begin to dilate. This dilation is caused by a direct local effect
of the cold on the vessels themselves-probably paralysis of the
contractile mechanism of the vessel wall or blocking of the nerve
impulses coming to the vessels. In any event, at temperatures approaching
0 degrees C. the vessels frequently reach maximum vasodilation. . . . .
." (p. 301-2)

Granted, this was describing skin (blood) vessels, but I would presume
vessels deeper within would follow the same general pattern. And of
course, we wouldn't want that temperature to get anywhere near freezing
the tissue. But perhaps we need not be in so much fear about
vasoconstriction impeding incoming oxytocin for MER.

At the ILCA conference in 2000, one speaker gave the report of her pilot
project using cold for engorgement (as physical therapists use for
swelling in all other body tissues) she used test weighing to check milk
transfer and concluded that intermittent cold packs (with appropriate
cloth protection between cold and skin) did not prevent the MER from
happening.

Another interesting factoid I found on p. 316 ff: lymph capillaries are
not constructed like circulatory capillaries,  nor do they work the same
(i.e. such as contracting/expanding with cold/heat). . . . "special
structure of the lymphatic capillaries. . ..the edge of one endothelial
cell simply overlaps the edge of the adjacent one in such a way that the
overlapping edge is free to flap inward, thus forming a minute valve that
opens to the interior of the capillary. Interstitial fluid, along with
its suspended particles, can push the valve open and then flow directly
into the capillary. But this fluid cannot leave the capillary once it has
entered because any backflow will close the flap valve."

In my view, it is this 3rd compartment or 3rd space/type of fluid that
has not yet entered into the lymph capillaries that seems the most
difficult to manage. Indeed, when vacuum is applied, this interstitial
fluid can be moved in the direction of the vacuum, making matters worse.

What if we could find some pro-active ways to encourage this fluid to
travel away from the breasts, into the lymph vessels more quickly,
develop some inward/upward massage strategies to teach moms.

Perhaps the old-fashioned heartburn/lactation exercise might get the
large pectoral muscles helping to pump more of it toward the deeper
lymphatics.

Maybe we could lessen the volume and duration of overall engorgement so
that is doesn't distort the nipple-areolar complex so radically and just
generally complicate early breastfeeding quite so much. It is into this
larger category that I feel RPS (see archives) fits.

Well, this is long enough and I am due at WIC in 45 minutes. I'm curious
what others think about my logic.

Jean
****************
K. Jean Cotterman RNC, IBCLC
Dayton, Ohio USA

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