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> I just came across this on another email list:  any comments on the
> truth of this, vets out there?
>
>
>     "If you are a cattleman, I am sure you are familiar with Grass
> Tetany and Milk Fever, and the sudden death associated with its
> occurrence. These were once thought to be magnesium and calcium
> deficiencies. We now know it is from high potassium forages and grasses.
> Similar situations causing abortions and gut problems often occur in
> horses. What happens is that the potassium spikes during cool, wet
> conditions and especially after long droughts followed by rainfall and
> rapid growth.  - Situations like frost and freezing are especially bad -
> have you ever had horse colic after a frost?  Probably so...the reason
> is a sudden mineral change in the grass, not just frozen grass! During
> these times sodium, calcium and magnesium decrease, while potassium
> increases. This spike in potassium is often deadly.
I think this is a valid comment, but not regarding milk fever.  The
progression of milk fever in cattle is well worked out, and does not
involve any change in feed or potential for a potassium spike.  In short,
cattle with the potential to milk heavily that are maintained on high
calcium feeds (the usual culprit is alfalfa hay) during their dry period
have their production of the hormone calcitonin suppressed by the ready
availability of calcium in the diet.  (Calcitonin is a hormone produced by
the parathyroid glands that enables rapid mobilization of calcium out of
bones in the face of a sudden need for it.)  When they begin to produce
milk in high quantities, there is a very sudden need for more calcium, and
without calcitonin present in sufficient quantity to mobilize it rapidly,
the cow becomes hypocalcemic to the point of collapse and death.  When
cows are fed low-calcium forages during their dry period, they have
sufficient calcitonin to mobilize calcium at the onset of lactation, and
do not suffer from this problem.

I do suspect that the same sort of mechanism is at work in endurance
horses who become hypocalcemic during work, and I've heard others (Jeannie
Waldron in particular) lecture on this same concept.  When they have ample
calcium available in the diet day-to-day, they don't rally sufficient
calcium in extreme exercise situations, and the result can be a gut
shut-down with an ileus.  However, these cases respond promptly to the
administration of calcium, and typically don't show the sort of anterior
enteritis that these horses exhibited, with the ongoing reflux during a
slower recovery phase.  The one really classic hypocalcemic case I had the
opportunity to treat was clinically essentially normal within about 10
minutes of receiving calcium, and had no reflux.  (I suspect he MIGHT have
had reflux had the calcium not been administered when it was--but I also
would wager that the reflux would have been due to strictly a
physiological blockage and would likewise have stopped as soon as the gut
resumed motility.)

I am more inclined to suspect forage changes due to the freezing in the
cases under discussion, as we DID have freezing conditions not long before
this ride at the higher elevations here in Idaho.

I'd also be curious to know what the electrolyte protocols were on these
horses, as it is under these sorts of conditions that I suspect we can too
often over-electrolyte.

Heidi



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