Sorry but I'm going nomail again for a while, but before doing so thought
I'd add to the discussion of cabbage and a few other odds and ends:
I'd agree entirely with KGA et al after having an accident in Nigeria in
1992 (only my padding prevented a broken leg) in a situation where no ice
or any compression or elevation was possible. The massive damage was above
the knee but swelling was so great that within a few hours I could not bend
the knee at all. Next day I could hardly walk, but spotted cabbage on a
roadside stall, insisted the driver stop, swathed the most painful bits and
the knee in cabbage, held loosely in place by stockings. A couple of hours
later the knee was bendable. As resolution occurred it was easy to spot the
area where cabbage had covered the bruising: this turned yellow a day or
more ahead of areas not covered by cabbage, still dark.
As for coleslaw: shredded cabbage was all I could get at the Hyatt Regency
Resort in Arizona in 1995 when experiencing an acute episode of
non-lactational mastitis. It works, but not as well as smooth cabbage leaf:
leaves a most peculiar resolution pattern because so much of it does not
touch the skin closely. However, combined with full-body immersion therapy-
hot spa and cold pool alternating- this mastitis resolved beautifully,
leaving only a large cyst needing to be drained by needle aspiration under
ultrasound. I strongly recommend anything that helps lymphatic clearance,
like hydrotherapy and skilled massage.
Cabbage is recommended as a poultice for any swelling. We even have
experience of it with bilateral hydroceles: worked well, I was told. Try it
on any soft tissue damage with unbroken skin and see. Great for fibrocystic
breast disease pre-menstrually, in my experience.
Re anaemia: long known to be associated with increased infection rates, but
also with other manifestations of decreased immune competence; so whether
the cause of the mastitis was obstructive or infective it would be likely
to manifest more strongly and be harder to resolve in the anemic mother.
But I would consideer it an unlikely CAUSE of mastitis, merely an
inevitable adjuvant.
And one last thing re milk production: we need to be careful in our
enthusiasm about autocrine control that we do not lose sight of the
importance of an adequate hormonal milieu for milk production. It is not a
matter of autocrine versus endocrine control, or endocrine followed by
autocrine control. The two mechanisms are at work throughout lactation, in
varying degrees of importance and in highly individual ways in women. Basal
prolactin levels may indeed drop over time, but I thought that
suckling-stimulated prolactin rises remain and in some way can be very
important to maintaining production as well as lactational amennorrhea.
(Hence we meet those mothers of prems, producing large volumes for weeks
and months but deprived of skin contact with their babies: volumes taper
off over time but respond dramatically to prolactin-stimulating drugs.) The
range of "normal" prolactin levels can vary widely in women all
breastfeeding successfully; so too can the range of prolactin levels needed
for adequate milk production. It is unlikely in any mother who has constant
physical contact with her baby that prolactin or other hormone levels will
be the problem causing undersupply: drainage is far more likely to be the
problem in such mothers. But even these include a few for whom hormonal
inputs can dramatically reduce supply, because they drop below whateveris
their personal critical threshhold for good milk production, even though
the milk is all being emptied. I've seen this in women on OCs among others.
Yes, even the mini-pill. (And we all know, thanks to Peter Hartmann, that
the emptier the breast, the faster the rate of milk synthesis.)
It's certainly true that prepartum and in the first few days endocrine
controls determine breast development and lactogenesis. It's also true that
there is some correlation between early prolactin levels, milk output and
infant intake, but that this is not evident after day 15 or so: women with
maintained hyperprolactinaemia do not have babies that grow better, or
greater milk volumes, than controls: they simply lose the
suckling-stimulated prolactin rise typical of ongoing lactation. It's true
that autocrine control gradually kicks in anytime from 20 hours onwards as
milk is synthesised in greater ammounts; and this inhibitory peptide
becomes a rapid feedback response mechanism that can determine milk
production. Both endocrine and autocrine systems are important at all
times, just in varying degrees. This is all discussed in the WHO book,
Infant feeding, the Physiological basis, available from ILCA and I strongly
recommend it to all Lactnetters who haven't a copy. (Start reading at
chapter 2 though.) And of course Peter Hartmann's two JHL articles. And
read Mavis Gunther's classic workj on mastitis if you can find her book,
Infant Feeding (1970).
This is all highly relevant to cases like that reported of the mother with
bilateral augmentation, localised mastitis and a baby that is still getting
enough milk to grow. Involution of any not-draining glandular tissue will
occur naturally. Milk production will continue in the draining areas of the
breast. There is no need to wean, to put her on antibiotics, or to do
anything other than try not to further damage areas of the breast which are
not draining and must involute. Cabbage and cold is great here. If enough
breast tissue doesn't work, supplementation may need to be considered
eventually. But remember the average total 24hour intakes of thriving
breastfed babies: day 1: 37ml; day 2: 84 ml; day 3: 266ml; day 4: 385ml;
day 5: 540ml; day 28: 750ml; 4 months 750ml. Some of these mothers can't
manage the increase needed between day 7 and day 28, but many of them have
enough in the first week. They need follow-up after discharge.
Maureen Minchin
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