HYPOCALCEMIA IN LATE-GESTATION (and lactating) DOES:
Feeding to Prevent it
By Sue Reith (2/07 update)

Hypocalcemia is a life-threatening condition that shows up when a doe is either pregnant or lactating, but getting fed an unbalanced diet that doesn’t provide her with enough calcium for both herself and her growing fetuses or for milk production.  It can appear at any time during the last 2 months of pregnancy, right up to the doe’s due date, as well as at any time while she’s lactating.
Symptoms:  The first thing she’ll do is refuse to eat her grain. Soon after that she won’t want her hay either.  Without quick intervention she’ll become weak and wobbly, lethargic and depressed. If still untreated by then, she’ll lie down and not want to get up. If you take her temperature when you first see these changes, it’ll be normal (102.3), but soon after that it’ll drop to sub-normal (below 102). Unless corrective measures are begun right away you’ll lose both the doe and her fetuses.
Treatment: If, because you’re unsure as to why the doe is behaving this way, you call a veterinarian in for advice, he or she will probably (and unfortunately) tell you that her problem is “pregnancy toxemia”, or “pregnancy disease”, or perhaps the most likely diagnosis will be “ketosis” a secondary condition that happens when the doe stops eating (in this case because she’s too weak to do so) thus has to start living on her own body’s reserves*. While ketosis was not the initial cause of the doe’s difficulty, after a couple of days  of being too weak to eat any food it will certainly become a major part of her problem! So it, too, must be dealt with fast!  A veterinarian, recognizing the ketosis but not the hypocalcemia that caused it, will want to treat with glucose, etc.  But it’s absolutely essential that the doe be treated with calcium supplements** at the same time, without which she will either end up dead, babies and all, or with a c-section, with babies too young to survive, and a hefty vet bill as well.  So it behooves the owner to take charge of this whole process right away, to treat the doe with calcium supplements for the hypocalcemia, and, if more than a day or two has passed before treatment was begun, with glucose for ketosis as well.

Cause:  It’s all about the food!  Most cases are seen in does that are getting a hefty grain ration along with their hay, especially when they’re getting grass hay instead of alfalfa. During the last 2 months of the doe’s pregnancy, this type of grain/grass hay diet does not provide enough Calcium for both the fast-growing fetuses’ bone development and for her own muscle tone as well, so depending on how many fetuses are draining calcium from her to build their little skeletons, at some point the babies will drain ALL of her calcium from her for their own needs, leaving her nothing to keep her heart going (the heart is a muscle) or to go into labor (the uterus is ALSO a muscle).  And the more fetuses she’s carrying, the sooner this will happen!  With just 1 or 2 fetuses she may make it until she goes into labor, but then be too weak from lack of muscle tone to expel the babies in a timely manner***. Or if she  does succeed in birthing the kids (often requiring the owner’s assistance), starting lactation in a calcium-deficient state can lead to a sudden (and very surprising!) loss of milk production at some unexpected point during lactation.
Prevention:  You CAN prevent this, just by feeding your pregnant does a proper diet during pregnancy!  Pregnant does need a great deal of calcium in their diets, particularly in the last two months of gestation. That’s when the fetuses, now having fully developed all their little parts, focus all their energy on growing rapidly, and in so doing drain large amounts of calcium from the mother’s body. Calcium is only available in the diet if the doe is ingesting at least 2 parts (and no more than 5 parts) of calcium-providing food to every 1 part of phosphorus-providing food. “The calcium-to-phosphorus ratio of a food or supplement determines how much of the calcium is absorbed.” (http://www.askdrsears.com/html/4/T040600.asp, bottom of the article, #8 under “12 ways to boost your calcium”.)
The only really good Calcium-providing feeds are alfalfa and clover, because grass hay contains barely any at all. OTOH, ALL forms of grain contain a great deal of phosphorus (and almost no calcium whatsoever). So if you feed grain without the calcium available from alfalfa or clover, OR if you feed alfalfa or clover without the phosphorus available from grain, there will be NO   calcium available in the diet you feed for the developing babies….
During the doe’s pregnancy, there are three basic feeding approaches that will prevent hypocalcemia.
(1)  Provide her daily with a small amount of grain (for a mature dairy-sized doe that would be no more than one cup per feeding) along with a regular ration of alfalfa, or,
(2)  If feeding a grass hay or pasture instead of alfalfa, give her NO grain at all. That’s because while grass hay does in itself contain a proper ratio of calcium to phosphorus, the total amount of each is exceedingly low.  But adding a heavy-phosphorus grain ration to it would turn the balance of calcium to phosphorus upside down to something like 1 Ca to 4 (or more) P, making NO calcium available to the doe, and setting her up for hypocalcemia in late gestation. To increase the availability of Calcium in this instance, provide a good free-choice loose supplemental trace mineral mixture that contains at least 16% protein (grass hay has only ~5%), along with a ratio of no lower than 2 parts of Calcium to each 1 part of Phosphorus (the amount of which could be nicely increased with the addition of powdered Di-Calcium Phosphate, available through feed suppliers as well as online.)
(3)  For those who would prefer to feed both grain and hay in late gestation, but because they don’t have ready access to free choice alfalfa must instead either pasture their goats or feed them grass hay,  if alfalfa pellets can be bought locally at a reasonable price, a perfect late gestation diet for prevention of Hypocalcemia would be a ration of 1 cup (by measure) of grain, added to (using the same cup) 3 cups of alfalfa pellets, fed 2X daily, along with all the free choice pasture or grass hay the does want to eat between meals, and free choice access to a good, loose, trace mineral supplement, and baking soda.
In an effort to help owners figure out just how much of what feed to give their late gestation does to provide that minimum 2:1 ratio, I recently wrote a technical nutritional analysis of how the 2 CA to 1 P balance works out in real-time farm-feeding measurements. (I’ll be happy to forward a copy of that analysis to readers who’d like to read it.)
And then to translate the technical information in the article into useful terms, I calculated the actual weight of the (minimum) 2Ca:1P ratio diet I feed to my own Togg does. In so doing I found that at mealtime they each get 1 lb of alfalfa (a combination of 12 oz alfalfa pellets, ALL of which is devoured eagerly, and roughly 24 oz loose alfalfa free choice, some of which is generally wasted) along with 1 cup (1/4 lb by weight) of grain. That’s roughly a per-meal ratio of 1 lb of calcium-containing food to each 1/4 lb of phosphorus containing food, translating to a daily ration of 4:1 (4 Ca to every 1 P), well-within the parameters of the acceptable calcium to phosphorus ratios of 2Ca:1P to 5Ca:1P that are needed to make calcium available in the diet.  
Because when measuring them pound for pound we can see there’s a difference in the volume of grain and alfalfa pellets, after calculating the above feeding ratio by weight I went back again and re-calculated it by volume.  When I filled up my 1-cup grain-measuring container with alfalfa pellets instead, I discovered that it took exactly 3 of them to fill up my larger, alfalfa-measuring container.  So, when measuring out a feeding of grain and alfalfa pellets for one animal, to provide the essential minimum of 2 Ca to 1 P ratio in that meal all you need to do is put 3 of the small scoops (or a larger scoop that holds the equivalent) of alfalfa pellets into the dish, and top it off with 1 small scoop of grain****! 
Addendum: For readers that while feeding to prevent Hypocalcemia are concerned about other nutrients, such as protein, being available to their does as well, according to Ensminger and Olentine’s Livestock Feeds and Nutrition Complete the average digestible protein content in grain is 11.2%, whereas in alfalfa it’s 15.9%, in clover 10.5%, in beet pulp it’s 14.1% and in grass hay 5.1%. The average digestible energy level in grain is 1.38%, in alfalfa it’s 1.13%, in clover it’s 0.93%, in beet pulp it’s 1.32%, and in grass hay it’s 1.8%. And, last but not least, the average crude fiber content in grain is 6%, in alfalfa it’s 27.2%, in clover it’s 25.7%, in beet pulp it’s 15.17%, and in grass hay it’s 28.2%.
Sue Reith
Carmelita Toggs
Bainbridge Island WA
suereith@msn.com
*When the goat doesn’t get food from outside, it tries to stay alive by using its own reserves.  Its own fatty tissue is used to provide energy, and in so doing it releases ‘ketones’ into the system.  The ketones soon shut down the liver, hence the name ‘ketosis’.
**The most effective calcium supplementation is done with CMPK, because it’s made up of not just Calcium, but also Magnesium, Phosphorus, and Potassium, formulated to work together as a team to make Calcium more quickly available to the body, and at the same time prevent an overdose of the Calcium (which when given alone can result in cardiac arrest) during restoration. For those that have no access to CMPK, A ‘homemade recipe’ for it follows: 

To re-create the equivalent of a 30 cc CMPK dose (650 mg calcium; 500mg potassium; 150 mg phosphorus; and 96 mg magnesium) right in your kitchen, go to the Supplements department of any large chain-type drugstore and buy a bottle of Posture-D tablets (containing 600mg calcium, 266mg phosphorus, and 50mg magnesium), and bottles of Potassium tablets (500 or 550mg) and Magnesium tablets (150 or 250mg).  Calculate the amount of each pill needed to come up with an equivalent to one 30cc dose of CMPK as spelled out above, and, using a pill cutter of some kind, create that amount, crush it up to a powder and serve it orally in a little yogurt. Or add some water to the mixture and dose it in a drenching syringe.
***This delayed labor brought about by a lack of sufficient calcium to provide the uterus with proper muscle tone is also the cause of Floppy Kid Syndrome!  The babies remain in the birth canal for too long before gaining access to oxygen, a process which sets up an acidosis in the brain tissue.  This is why Sodium Bicarbonate is the treatment of choice to save the ‘Floppy Kid”, which it does by neutralizing the acidosis in the kid’s brain.
****If the pregnant doe is lactating and still being milked, you can serve that grain/pellets combo to her while in the stanchion
Sue Reith

Lets talk about CAE.

At the very beginning of my Kinder breeding program I was just like lots of others, looking for more genetics for my Kinder herd without using caution when buying new stock for that program.

Sure I had read all the warnings of bringing in new stock without asking about CAE, CL and etc. but just as I have already stated, I threw all caution to the wind. All I could think about was wanting new bloodlines to increase my gene pool.

Well in 1994 the chickens came home to roost, so to speak. After coming back from the Missouri State Fair, with a blue ribbon for the Kinder doe that milked the most in the milking competition, it was time for CAE testing. This was the first time for my testing the doe that had won the milking competition. It was then that my night mare started.

I had the vet to come and draw blood for CAE.The vet called when he received the test results. All negative except for one doe. This was the doe that had won the milking competition. This was the one that tested positive for CAE. I will always remember how sick I felt. I could not believe this, she didn’t have enlarged knee joints, she was in great condition and her coat shown like a bright new copper penny. There had to be some mistake, the test had to be wrong. So I ask the vet to draw more blood and send it to another lab.

I held my breath waiting for those results but no amount of wishing was going to change the results of the first testing. The doe once again tested positive. Just hoping against all hope I ask to have more blood drawn and sent to a third lab. The results were the same, positive for CAE.

What was I going to do? Not only did I have a CAE doe in my herd but I had put all the rest of the herd at risk. I would not be able to sell Kinder; my reputation was ruined. No one would ever want to buy a Kinder goat from me. My time for breeding Kinder seemed to be at an end. I was sick and sick at heart.

I called a friend in the Kinder Association and confided in her. She convinced me to do what every lab had suggested. Put down the doe with CAE then use CAE prevention with all the other Kinder in my herd. This would mean that I must be there at every birth and never allow a doe to touch any of her kids. I would need to heat treat the colostrum and pasteurize all the milk then bottle all the kids. The labs had told me that I would need to do this for some years because, even if no other Kinder had tested positive for CAE, it could at any time raise it ugly head again. The one doe had CAE and I had exposed all the others to this monster.

We put the doe down that had CAE, then my work began to try to stop CAE from infecting my other animals. It was lots of work and heart breaking to never let a doe see her babies. When Harvey would come to evaluate and even mention that a knee joint might be a little enlarged I would immediately send that animal for meat. We tested every year for CAE.

Years passed and never another animal positive for CAE. My life breeding Kinder did continue. My reputation had not been destroyed and I watched with such pride with many does being first in their class, winning championships and winning stars in one-day testing.

What is my point for writing about all this? I want to tell others how important it is to ask questions when buying animals. I want to impress on everyone that you cannot be too careful. It is important to have a gene pool but not at the expense of all your herd. It would have been so much better to have had fewer genetics than to expose all my goats to CAE. It didn’t wipe out all my Kinder but it surely could have. God was good! It was only by the grace of God that I was able to continue my Kinder breeding. Breeding Kinder goats is something that I have just loved since the very first day and I am so thankful for the experience to have done that. I always keep in mind that it was almost cut short by my wanting more and better genetics. Be very careful!

Abnormalities and all sort of disease like Johne’s, CAE and CL can quickly deplete the Kinder gene pool. Selling animals with any of the above will decrease the gene pool all across the country. Great care needs to be taken when selling animals and when buying stock from others.

This is true of all breeds but the Kinder is much more vulnerable because their gene pool is so small compared to the other breeds.

We need to be vigilant in our breeding practices so we sell only animals with good genetics, those that are healthy in every way and those that conform to the Kinder Breed Standard.