Lisa wrote:

<I'm having an up-close-and-personal experience with the edema phenomena
with
my sister, who just gave birth by c-sect after PROM to twins at 34wks. She
was already having problems with her ankles, but nothing like now!  She says
that the edema started to increase after she received pain and anti-nausea
medications post-surgery (she had a rough recovery; the medications made her
sick) and her perception is that they caused the problem. Water had broken
at midnight, she went to the hospital and was put on IVs but no pit, no
labor, prior to surgery at 9am. Edema became worse within 24 hours after
delivery.>

Witte and Witte quote Starling, the brilliant physician who figured out
edema formation, as saying that edema results when the rate of interstitial
fluid formation exceeds the rate of removal.

Unfortunately, the # of hours she had IV's before her CS doesn't tell us how
fast it was administered, nor how many total bags of fluid she
had, including preparation for the anesthetic. The epidural or spinal itself
was probably preceded by a bolus of fluids for BP control, plus further IV
support necessitated by the surgery itself, including any keep open IV's,
probably with pitocin, and for how many hours after birth.

You describe her having prenatal edema, some of which could be partly due to
gravity, pressure of a twin-pregnant uterus on her lower extremities, plus
the normal changes in colloid osmotic pressure that occur in pregnancy and
after birth, which research has shown to cause fluid shift in normal
pregnancy/birth without interventions.

So we can only presume that she was probably not actually dehydrated before
she was admitted. The IV"s begun on admission were probably to prevent
subsequent dehydration, and perhaps to administer prophylactic antibiotics
due to PROM.

Who knows at just what point her tissues began to contain more than 30%
above the normal amount of interstitial fluid, the amount at which pitting
begins to show up? All IV fluids from that unknown point onward would
probably begin to create visible edema that the mom could perceive. But it
was building up even before she perceived it, and without knowing any of
this, it is understandable that she connected it with the events she could
remember close to the time she noticed it.

From my reading, I have developed a general rule of thumb: The more total
bags of IV fluid a mom receives, especially the longer before birth they
were started, the more likely she is to have noticeable edema, in which the
breast, of course, shares.

I had been observing, looking up references and thinking over this
phenomenon for the several years when I was writing the JHL article on RPS.
I came across one reference that, while it did not include maternity
patients, did test various types of IV fluids on adult male and
female surgical patients of widely varying ages, to prevent /treat shock.
The statement was made, something to the effect that at least, in these
types of situations, every bag of IV fluid takes 2-5 days to leave the
interstitial fluid and be eliminated. Unfortunately, I guess I didn't keep
the citation.

<  . . . . .  At 11 days postpartum, she tells me that
it has improved "a little."  . . . . . . As I'm talking to some of my other
colleagues, I'm finding that this
keeps-getting-worse thing is not uncommon. I do not know how much pitocin
may have been given to her postsurgery, and I don't think it is just the IV
fluids; she should have long ago peed that all out. >

Not necessarily, if any of that previous reference applies, because we don't
know just how many bags of fluid total she received. The total amount of
pitocin makes a difference too, some doses more likely to act as an
antidiuretic than others.

<Either something is upregulating ADH receptors big time or some similar
process that does *not*
reverse quickly. Onset more than a day *after* delivery, increases in
severity for the next few days, then takes 2 or more weeks to resolve.>

Again, we do not have any accurate idea of her total IV intake, let
alone her oral intake, or the insensitive water loss through perspiration
and respiration, nor her urinary output, to begin to go by. I know that 24
hour intake and output records were difficult to keep accurately four
decades ago when I worked in OB.  I wonder how much of an effort is made at
the current time to keep at least the IV intake accurately recorded?
Lactnetters who currently do nursing care on OB units would be a better
judge of the trend.

< What puzzles me is that I don't think her exposure to pitocin was very
extensive,>

Again, we don't know precisely. Any L&D nurses on the list to give us a clue
as to whether each ampoule of pitocin added to IV's is faithully recorded so
that there would be a "paper trail" for anyone wanting to include this
factor in research??? This whole phenomenon certainly would make a very
challenging research project for a masters thesis in nursing!


<and that's the only potential connection I know of so far.>

<Does anyone have any other ideas on what may be causing this postpartum
edema besides the pitocin theory? I'm interested in any insights from those
who notice and follow these things.  There has GOT to be a connection here
somewhere. I just don't remember this happening like this to mothers a
decade ago.>

Actually, sounds lucky that she didn't end up with pulmonary edema, what
with all that fluid retention! How has it effected her milk production rate
and her success with pumping for the twins???


Though much of what I found was definitely over my head, I was able to gain
some insights from quite a few of the references that I found. This is just
a small sampling:


<Han JS, Yoshitaka M, Knepper MA, Dual actions of vasopressin and oxytocin
in regulation of water permeability in terminal collecting duct, *Am J
Physiol, July 1993, Vol 265, Number 1, F 26-34.*

*          * "Oxytocin, like vasopressin, has dual effects on osmotic water
permeability, increasing it at subnanomolar concentrations and inhibiting it
at suprananomolar concentrations . . .The inhibitory effect on water
permeability is associated with binding of vasopressin or oxytocin to either
an oxytocin receptor, a novel vasopressin receptor, or both."





Chou CL, DiGiovanni SR, Mejia R, Neilsen S, Knepper MA, Oxtocin as an
antidiuretic hormone I. Concentration dependence of action, *Am J Physiol
(United States),  Jul 1995, 269(1 Pt 2)* p F78-85.



Chou CL, DiGiovanni SR, Luther A, Lolait SJ, Knepper MA,  Oxytocin as an
antidiuretic hormone II. Role of V2 vasopressin receptor, *Am J Physiol (United
States), Jul 1995, 269 (1 Pt 2)* pF70-77.





Witte, CL, Witte MH, On the Causation of Edema: A Lymphologic
Perspective. *Perspectives
in Biology and Medicine, 41, 1 Autumn 1997, pp. 86-97.* (This one in
particular, was relatively easy to understand and very helpful in
understanding the whole phenomenon of edema in general.)



Guyton AC, Basic Human Physiology: Normal Function and Mechanisms of
Disease, Second Edition, 1977,W.B.Saunders Co. Philadelphia (Same address as
below) There was a third edition in 1979, I think.

          ". . .an increase in extra-cellular fluid volume is associated
with an increase in blood volume of about one-fourth to one-third as
much-that is, until the extracellular volume rises above 20-22 liters. The
remainder of the extracellular fluid is distributed to the interstitial
sapces. However, when the extracellular fluid volume rises above 20-22
liters, very little of the additional fluid will remain in the blood-almost
all of it instead going into the interstitial spaces. this effect occurs
when the intersitial fluid pressure rises from its normal negative value
(subatmospheric) to a positive value, because the compliance of the tissue
spaces then becomes tremendous, so that they can then hold as much as 20-40
liters of fluid with very little additional rise in interstitial pressure.
Therefore, the interstitial fluid spaces, under these conditions, literally
become an "overflow" reservoir for excess fluid. This obviously causes
edema, but it also acts as an important overflow release valve for the
circulatory system, a well known phenomenon that is utilized daily by the
clinician to allow him to administer almost unlimited quantities of
intravenous fluid and yet not force the heart into cardiac failure." Pp.
361-362



This phenomenon of edema, as separate from physiological engorgement,
definitely needs to be researched, especially in relation to its effect on
lactogenesis II and the comfortable initiation of breastfeeding. Some of the
best-known engorgement articles make little or no mention of it, and neither
the quantity of IV fluids nor the amounts of pitocin administered were
considered as significant variables, even though these articles were
written well into the years that perinatal medicine was gaining a firm
foothold  and IV intervention was becoming standard practice. These
practices took place slowly enough that just a few more mothers per month
exhibited edema. With turnover of OB staffs and rotating residencies, people
working in OB eventually began to take the presence of edema as "normal".
The change is very obvious to those who left hospital practice before these
interventions were so routine.





Moon JL, Humenick SS, Breast engorgement: contributing variables and
variables amenable to nursing intervention, *JOGNN *1989;18(4):309-315.



Hill PS, Humenick SS, The Occurrence of Breast Engorgement, *J Hum Lact *10(2),
1994, p. 79-86.



Humenick SS, Hill PD, Anderson MA, Breast Engorgement: Patterns and Selected
Outcomes *J Hum Lact 10(2), 1994, pp. 87-93.*

**

**

Jean

******************

K. Jean Cotterman RNC, IBCLC

Dayton, OH USA

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