<I remember hearing something a while back about pitocin delaying milk coming
in.am I right on that?  If so - can anyone point me to information on this?
Mom is determined to nurse these babies.  :-)>


Jaye,

These are some of the things I know about pitocin. Not only does it help contract the uterus, but because it's molecular chemistry is very close to that of another posterior pituitary hormone ADH (antidiuretic hormone) it has the ability to attach to the same binding sites as ADH. Therefore, in certain doses, it has an antidiuretic effect on the kidney. 



This means the body will retain some of the IV fluid longer than if there were no, or no large amounts of pitocin involved. It takes some imagination, palpation and experience to assess the various components of postpartum breast swelling. This is my interpretation of what the various components of sometimes even intrapartum, and postpartum breast swelling are due to:



1) circulatory expansion (in response to placental hormones leaving the circulation after placental birth). This will allow for delivery of prolactin, insulin, and other hormones and raw materials that together will bring about the initiation of L-2, when appropriate amounts in the right proportions reach the basement membrane of the milk making cells.



2) Pre-L2 edema: my term for early retained fluid in the interstitial tissue due to large amounts of IV fluid and additionally, slowed diuresis from pitocin, and 



3) actual newly manufactured and perhaps, ineffectively removed milk.  



4) Post L2 edema, my label for the further edema backed up by pressure from the stasis in the swollen, inadequately drained glandular system, which can then crowd the venous and lymphatic circulation process whose function is to remove waste materials and excess interstitial fluid back into the circulation.

 

This last kind of swelling is what was described 25-50+ years ago, with delayed and scheduled and restricted breastfeeding, routine supplements, back in the days before perinatal medicine introduced widespread use of IV fluids and often more than the standard dose of 1 cc. of pitocin I was seeing all mothers in our delivery suite getting even back in 1948. 



Or her swelling could be a combination of all of the above. Engorgement in our present day and under today's obstetric management, has been poorly defined, often mischaracterized, and that needs semantic attention  from us all, and further formal research attention. And it seems to be taken for granted. So many HCP's, even LC's, even seem to consider it to be "normal" instead of iatrogenic. Without credible research, we will never be able to persuade our medical colleagues to take a second look at these sequellae of certain aspects of managed care, and possible alteration of some of them for the sake of better breastfeeding initiation experiences for mothers and babies.



You did not say how much total IV fluid she received. Many places do not consider this important information to track. I have observed that if a mother gets a total of oral and IV intake of more than 1500 - 2000 cc. in any one 24 hour period, you can expect some breast edemabefore L-2. If she received IV fluids both before birth, especially for  long induction, for epidural boluses, and for 24 hours after birth, it may well be that there is enough intersitial fluid to slow down the transfer of raw materials from the arterial capillaries to the basement membrane of the milk making cells. So theoretically there could be some delay in the onset of Lactogenesis II for this reason. This point needs much more research, because it is so common, and it robs so many mothers and babies of a good beginning experience. 



However, you said that there was some milk removal. and you characterize the breasts as "stil full, but no significant milk." Or is it no significant milk yet seeming to be removable??? 



<My client is a first time mom with twins born at 39 wks - vaginal delivery -
had epidural and pitocin during labor.  Due to large uterus, Dr was
concerned about bleeding and put mom on a 24 hour pitocin drip.
 

Mom's milk supply has NOT come in - she is pumping regularly and is getting
only 5 mls from each breast.  We are looking at hormone levels and getting
testing done as she did have unexplained fertility issues and it took 5 yrs
to get pregnant (in-vitro).  She had appropriate breast growth during
pregnancy - has no issues with hypoplasia - and had the full breasts about 5
days after delivery when she thought her milk was coming in.but it didn't.
Breasts still full, but no significant milk.>



This is the possibility that comes to my mind about your client. It is important to remember that:



When a mother has excess interstitial fluid in the breast, it can be thought of like a flood in nature. Unlike the blood, and lymph, which are contained in the blood and lymphatic vessels, or milk, which is contained within the lobules and ducts, the interstitial fluid ends up reminding one of a "rising swamp", practicaly without boundaries except for the skin and the walls of circulatory and glandular compartments. The more interstitial fluid there is, the greater the pressure within the tightly stretched skin. 



Vacuum does not pull. Other forces push. Breast pump engineers know that. LC's and the rest of the lactation community need to become well aware of that too when choosing interventions.



Vacuum often makes matters worse, as the crowding of the interstitial fluid pressure pushes the interstitial fluid itself forward into the flange of the pump, because "Nature abhors a vacuum." Pretty soon, the swelling in the subareolar tissues is enough to exceed and oppose the pressure of the MER, and any hydraulic pressure that the flange tunnel typically exerts on the ducts beneath the areolar skin. Therefore, even fingertip expression will be able to remove little or no milk, despite the fact that palpation of the upper outer quadrant of the breast reveals lobules swollen with milk, waiting to come forward, or eventually to start causing involution.



Gravity too effects the location of the interstitial fluid. If the mom has pendulous and/or very swollen breasts, and spends much of the 24 hour day in an upright position, gravity will attract excess interstitial fluid downward toward the anterior breast and the nipple-areolar complex. 



Your account makes me wonder whether these factors, more than hormone levels etc. are at play,



My suggestion is to have the mother spend more periods lying essentially flat, with a pillow, so that the breasts are on top of the chest wall. This allows gravity to attract interstitial fluid in its natural pathways toward the lymphatic vessels and venous capillaries leading it eventually back to the heart. Our colleagues in the lymphatic drainage field could no doubt give some suggesions on gentle massage of the upper lymphatic pathways to begin clearing them, etc. for better drainage of edema from the breast.



While she is in this position, application of reverse pressure softening, 60 seconds or even at first up to 5-10 minutes of steady, firm but not painful positive pressure on the areola all around the nipple will move much interstitial edema out of the subareolar tissues moving it further back up into the breast, temporarily. RPS will also trigger the MER. After the areola is temporarily softened, a short session of pumping on medium vacuum can take place, for no more than 5-7 minutes or so or till the milk begins to slow down. Time for a short break for gentle forward massage of the milk from the back of the breast, possibly back in a recumbent position again. Then, repeat that whole cycle 3-4 times if desired. IME, this often allows for some significant milk removal while helping keep some of the edema "at bay" temporarily so that milk, helped by external massage can push its way forward to equalize the cycles of vacuum within the flange area.



For mothers whose babies would be going to breast, this same set of insights can offer a window of time for more effective latching, in a "laid-back" position, using gravity of the baby's head to maintain the latch more easily.



Since I am not capable of academic research, these are my empiric observations from decades of direct clinical practice, backed up by reading in many fields. I welcome any feedback, negatve or positive. I encourage everyone to help spread what insights we gain from clinical practice, and encourage further formal research to disprove those observations if they are in fact inaccurate.



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


Chikly B, Lymph Drainage Therapy: Treatment for Engorgement. Presented at International Lactation Consultant Association Conference, Aug. 2, 1999, Scottsdale, AZ. Audio tape: Repeat Performance 219-465-1234..

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.

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