Ivy writes about a mother in her care who has had a very severe complication:

<Hi everyone,
This is my first post. I am an IBCLC in Beijing, China, helping a
previously healthy 25-year-old mom who developed acute fatty liver disease
at the very end of her pregnancy. It was not diagnosed until she gave birth
by cesarean at term 15 days ago. Baby was hypoxic, had aspirated
meconium-stained amniotic fluid, was resuscitated and sent to NICU and is
still there overcoming pneumonia, pulmonary hemmorage, kidney failure.
Mom's life was in danger until just 5 days ago. She has been jaundiced and
had severe systemic edema due to being in IV meds while kidneys were
recovering from damage. Liver function is finally stabilizing and she is
starting to be able to move around. She really wants to breastfeed but was
not able to start Pumping until today.  She expressed three times and got
just a few Milliliters.

Does anyone have experience working with such a mother to relactate?  Both
may be discharged in a week.>


I have deliberately waited to see if someone with such experience would answer.
 

I hasten to say that I do not have any experience helping such a mother breastfeed. But I have done a great deal of thnking about the need for more insight into such cases. This is because mothers with severe complications requiring heroic lifesaving measures, especially large amounts of intravenous fluid, will continue to need expert lactation management. This will continue to be so even if practices could be changed for mothers who experience no complcations, or only minor problems. 


(But this would require that we successfully demonstrate to all obstetricians and anesthesiologists the connection between difficulities in initiation of lactation during the first 7-14 days when mothers receive excess IV/oral fluid, e.g.< 2000-2500 cc. in any 24 hour period before or after birth, especially when IV pitocin is administered for many hours for induction, augmentation or 3rd stage management). (I am reporting my own clinical observation and what I have read in anesthesiology references here. Much good research has shown that intrapartum IV fluid causes reduction in postpartum colloid osmotic pressure, (which can risk pleural edema, etc.) I am not aware that any research has been done as yet on whether reduced COP may or may not effect lactogenesis 2.)


At 15 days, I think this situation needs to be thought of in terms of "delayed onset of lactogenesis 2" rather than as "re-lactating". Until her body chemistry began to normalize, the hormones and raw materials may not have reached the appropriate concentrations to cross through the cell walls of the lactocytes. Now, perhaps they can, and her breasts may well be able to begin secretion of at least some mature milk to replace colostrum that was collecting in the ducts from mid-pregnancy on.

 
I recall reading of such a mother several years ago, either in JHL or on Lactnet, or perhaps another source. But I am unable to give a reference. (I remember that she was strongly supported by her own mother who was either a LLL leader or an IBCLC or both.) The young mother had had such a hemorrhage that Sheehan's syndrome was feared. Much IV fluid plus blood transfusions were part of her care. I seem to remember that pumping was part of the plan and that at least partial lactogenesis finally began to occur around 12 days postpartum.


These are my thoughts:


1) Per private communication, an Australian midwife named Dawn Hunter once explained to me that several decades ago, it was part of routine care for certain blood tests, including an albumen level, to be drawn on new mothers. Her observation was that lactogenesis 2 never occurred until the mother's albumen level had returned to normal. I don't know if, or how much IV fluid these mothers may have received or whether normal postpartum fluid shift was responsible for resumption of normal colloid osmotic pressure in the plasma. Since this mother in Ivy's care had a problem involving the liver, it would be interesting to review her blood work to seek clues in her albumen level, or colloid osmotic pressure (no longer ever done in our town) or whatever similar medical testing may have been done.


2) Severe edema was mentioned, in relation to both kidney problems and IV's and IV meds, although pitocin was not singled out. No doubt the breast shares in storing some of the edema, especially if it is pendulous enough for gravity to attract fluid toward the nipple-areolar complex. It would be wise to examine the areola for edema each time before any pumping attempts, teaching the mother to use her fingertips to observe for this. (I tell mothers that the "milk ducts are surrounded by spongy, protective tissue, and can store a lot of retained fluid if necessary.") 
      * This tissue fluid is not "contained" in vessels or ducts and can disperse downward through the tissues fast 
         enough to have the effect of "burying" the subareolar ducts. 
      * If a pump is used when excess tissue fluid is present in the tissues, this edema will quickly and easily push its 
         way forward toward the vacuum area in nature's desire to equalize pressures. 
      * (In other words: Vacuum does not pull; other forces push.) 
      * This crowding of the subareolar tissues with interstitial fluid often delays exit of any colostrum/milk that may be 
         in the subareolar ducts. 
      * This crowding of the areola with tissue fluid may be enough even to prevent fingertip expression from 
         compressing the ducts despite normal amounts of colostrum waiting close beneath the nipple.  
      * I have found that Reverse Pressure Softening  (in an anti-gravity position if necessary) before and at 5-7      
         minute intervals during pumping or before fingertip expression, can displace edema temporarily to allow the ducts 
         themselves to be compressed to move milk forward to leave the nipple. 
      * (See www.kellymom.com/reversepressuresoftening/ or contact me privately for more information on reverse 
         pressure softening (RPS) if it is new to you.) 
      * RPS also always stimulates the let-down reflex, and I make a point of explaining the MER in simple terms so the 
         mother knows she can purposely use it as a tool to help milk removal.
      * Fingertip expression after pumping (as shown in Jane Morton's Stanford/edu videos on breastfeeding) may yield 
         even more total colostrum if any edema has been repeatedly displaced by RPS if necessary during milk removal.

3) At whatever point the baby is capable of oral feedings, if given by bottle, "pacing" the feedings while holding the baby in an upright position allows the baby more control by removing the force of gravity from the flow rate. Just as important, it familiarizes the baby with pauses so that s/he will not develop a preference for a constant "firehose flow" rate of feeding. Then when the baby is ready for direct latching, or latching with a shield, giving supplemental feedings while at breast (with a medicine dropper,dental syringe or a homemade or commercial supplementer inserted into the corner of the baby's mouth) gives the breast more stimulation and saves the mother time with simultaneous supplementation while breastfeeding.


Welcome to Lactnet Ivy. We will all anxiously await any updates one way or another from you, because case studies enable us to learn from one anothers' experiences, observations and insights.


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

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