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Discussion Starter · #1 ·
Tim finally kidded and I missed it- I checked on her at midnight then fell asleep and didn't wake til dawn.
She had 4- all doelings but two were dead when I found them. Sounds heartless but that is better I think. I didn't want to bottle feed and three tore up her udder last year. She would have tried to feed all I know but I couldn't have let her do that- no more even three. So I would have had to pull them and tried to find homes for them.
The two dead ones I don't think ever breathed because their airways were not clear- they were still warm so I tried to get them to breath but there was no response..
Now I have a problem with Tim- I had seen that she was laying down a lot towards the last couple of weeks but she would come for her grain and scratches so I thought it was just extreme preggoness. But she still won't stand for long- I found her on her front knees while the kids nursed (eventually-one just froze everytime I touched her so it took awhile to direct her to dinner) -I wonder now if her front feet are bothering her. After she rests awhile I wiill try to get her to stand while I see what I can see.
I don't think I will breed Tim again- at least for a couple of years- she's just tooooo fertile and so many babies are hard on her. Her first year she had two, last year three and this year four- I'm scared about next year- so she gets a good long rest.
And speaking of rest- I need to crash awhile myself.

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Discussion Starter · #2 ·
Tim and the two girls were up and about this afternoon- so not as bad as I thought. I think she has a bit of hoof rot in one front foot- it looks a bit punky but couldn't see anything else.
The girls (for the moment White Ear and Brown Ear) seem to have full tummys and Tim is being her usual good mom. She's still working the afterbirth out - having no problem with that.

I definitely have to rethink how I go about this- I need a better handle on when the birth is coming. She was not restless or having contractions when I checked her at midnight- She was lying in her usual spot, singing like she had been for two weeks- ligaments had long gone, babies dropped days ago- there must be a way of telling better. Never have seen a mucus plug with her. Simply checking every two hours for days is something I can't manage.

Thank goodness that Tim seems OK.

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glad Tim is up and around more adn the kids are acting satisfied.

It really can be hard on them when they are carrying that many kids.

Someone posted a thing by Sue Reith (sp?) about hypocalcemia on another site and I will post it here. That was all that came to mind when I read your post

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Discussion Starter · #5 ·
I read that too- it made me seperate the girls so Tim could go on straight alfalfa- I fed her alfalfa pellets and added crushed Tums to each meal. I also periodically dosed her with calium drenches. I'm giving her Cal-9-fresh now. But when it got sloser she refused the pellets and tums and only ate the hay.

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I don't know how I didn't see this too. I think its because the name was similar to another thread I'd already read and replied too.

Anyway, Congrats on the 2 healthy doelings and that Tim's doing better. Sorry you lost the other two.

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Glad to hear you at least have a couple live ones. I can honestly say I know how you feel on that one. I to(just a couple days ago) overslept and missed my yearling doe when she kidded. She had trips-two lively and one not. Thankgoodness though that she is being a good mom and is nursing her two surviving babies.

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Discussion Starter · #9 ·
I am lucky that Tim is such a good mom- that was what was so scarey- that I might have lost her by oversleeping.
She is doing better again today- the little kids are more lively and begining to explore.
I know one traditional Boer looks like another but pictures will come as soon as it stops raining and hailing.

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Hypocalcemia Articles by Sue Reith

• HYPOCALCEMIA Adjusting the diet to avoid it and to support fetal growth • HYPOCALCEMIA: HOW TO RECOGNIZE IT, TREAT IT, AND PREVENT IT

HYPOCALCEMIA Adjusting the diet to avoid it and to support fetal growth (Revised January 2004) By Sue ReithThe following information is designed to help goat owners avoid hypocalcemia in their pregnant does.
I encourage the reader to give the veterinarian a copy if one is called to help with a doe that shows signs of it. The fact is, does that come down with hypocalcemia are often raised as pets, family milkers, and/or show stock, and are likely to live where the only available vets are dog/cat specialists that don't routinely treat goats.
When presented with a pregnant doe that's exhibiting its classic symptoms, reading this information might help the attending vet to recognize hypocalcemia so that before making a diagnosis he/she can ask the owner a very simple question: "What type of feed, and how much of it, is this doe eating?"


January 2004) By Sue ReithFor those who don't know about hypocalcemia, it's a life-threatening condition that shows up when a doe's either pregnant or in milk, but eating an imbalanced diet that doesn't provide her with enough calcium for both herself and her growing fetuses, or for milk production if she's already lactating.

Symptoms: Hypocalcemia can show up in a doe any time in the last 2 months of pregnancy, right up to the due date, as well as while she's in milk. Most cases are seen in does that were routinely fed a hefty grain ration along with their hay during the 1st 3 months of pregnancy. The problem can start as early as the 4th month of gestation.
When it does, the first thing you'll notice is that she stops eating her grain. Soon after that she won't want her hay either. If during those 1st 3 months she was fed grass hay instead of alfalfa along with her grain, the chances are especially good that you'll run into this. If concerned enough to take her temperature when you see those first signs it'll be normal (102.3), but soon after that it'll drop to sub-normal (below 102).
Start corrective steps right away or she'll weaken fast and get wobbly, lethargic and depressed. If not treated by that point she'll go down and not get up again.

I first went through this back in the 1970's. When I fed, I noticed that one of my does was just lying there instead of hopping right up and eating with the rest, but I foolishly assumed she simply wasn't hungry and was only lying around because she was uncomfortable from lugging around all those babies inside of her. It took me a day or two to get concerned about her, and when I took her to the local dog/cat vet he didn't recognize what was wrong, so her turned for help to his veterinary guide (which did, and still does, lack any information on how to recognize and treat hypocalcemia), concluding from what he'd read in there that she had pregnancy toxemia. So he put her on IV Ringers until she died.

To avoid going through that expensive heartache, here's what you, the owner, can do yourself to repair your own doe when you see these first signs of hypocalcemia.
The meds dosages I'll mention are for full-sized dairy-type does, weighing ~ 120-150 lbs average, so if your doe is smaller you'll need to adjust doses for her:

Treatment: Right away (and trust me, speed is important!), give her Nutridrench or oral propylene glycol to replace that source of energy she lost when she stopped eating. This will prevent ketosis, a life-threatening metabolic condition caused by an animal's having to live on its own body reserves once it has stopped eating food. If this isn't corrected fast she can sink into a coma and die.

She should get either the dose of Nutridrench recommended for her weight, or 60cc (2oz) of propylene glycol, 2x daily for 2 days to restore her, and then 30cc (1oz) of that each day from then on until she's eating right again, to prevent/reverse ketosis.

Now let's turn to the primary problem, hypocalcemia. The fact is, we all need calcium for muscle tone. The heart is a muscle, and to keep it beating right the doe has to get enough calcium. So as soon as she's been treated to prevent ketosis, start her on replacement therapy to bring her calcium level back up to normal.
If you're having a vet help you with the repair process he may want to use Calcium gluconate for that. But CMPK will do a better job, because while calcium gluconate is just calcium, CMPK also has magnesium, phosphorus, and potassium in it, and they all work as a team to make the calcium available faster and more efficiently to the body, speeding up her recovery.
Also, there's a risk in using calcium gluconate by itself to treat hypocalcemia. "Too much of a good thing" can be harmful, and giving it too fast or in too big a dose will make her heart beat too rapidly, which could cause heart failure. When CMPK is used instead, the potassium in it slows down the heart rate, balancing out the calcium so the heartbeat will stay normal as the calcium gets returned to her system.
Important! Warm CMPK to body temp before injecting it! CMPK injectable is given sub-cutaneously (just below the skin) in the area between the last rib and the pelvis, at the rate of 30cc SQ, about every 2 hours until the calcium the doe needs has been replaced. We dose this way so we can continuously watch for improvement and easily tell when her system has returned to normal.

To check her progress, we compare her heart rate to that of a normal doe (70 - 80 beats per minute). At the beginning of the hypocalcemic doe's treatment her heart rate will be slower than that of the normal doe because she's so calcium deficient. When her heart rate is back up to the same speed as that of the normal doe, and she appears bright and alert and wants to eat again, things are going well.
However, giving your hypocalcemic doe just a single dose, or a few doses, of the CMPK will ONLY balance her calcium level FOR THE MOMENT, but as those babies continue to grow they'll drain more and more calcium from her, so after her heart rate's back up to normal it's very important to keep giving her DAILY MAINTENANCE DOSES OF ~ 30cc (1oz) of CMPK UNTIL SHE FRESHENS.

If you see signs that she's weakening again any time before then you'll have to increase the dose, but only temporarily, until she's OK once more. In my view the injectable form of CMPK is the best choice for treatment of the debilitated doe, because with it she can be dosed accurately, without a struggle. The problem is that while this form is the easiest to use and relatively inexpensive (about $4/1000ml in the catalogs), it requires a veterinary prescription.
The down side of this is that most veterinarians don't seem to know anything about hypocalcemia, nor understand why your doe needs continued doses of calcium. So being somewhat cautious they will only want to prescribe or provide a single dose, or perhaps two. That's like trying to fix a leaking dam by putting your finger in the hole.
All the more reason why you might want to share this article with your veterinarian of choice. (Editor's note: Many owners report their veterinarians refuse to even read this information. In that case, to save the life of your doe I urge you to go online fast and order the oral CMPK gel from a livestock catalog.

The gel, a non-Rx item readily obtained OTC and in catalogs, is a paste, and once placed in the doe's mouth will sit there until swallowed. One tube of 400gm (~14 oz) CMPK gel (~ $4) will provide a hypocalcemic doe with about fourteen 30cc doses.
If unable to find that, order the oral liquid CMPK or MFO instead, as they will both work well, dosed with a 35cc syringe. An udder canula attached to it will turn it into an oral dosing syringe. One word of caution: When using the oral liquid CMPK, it's important to dispense no more than one swallow at a time to keep the doe from choking, which could lead to aspiration pneumonia.
Either of these products can be shipped to you by next-day-air. If you need information about online catalogs contact me at [email protected].)

Once you get her calcium level back to normal and she starts eating again, your doe will probably still refuse grain for a while. Don't worry, because she's still instinctively trying to fix her calcium-deficient condition, and she's the best judge of that. She'll want to eat it again soon, and when she does it's wise to give her just a small amount of it at each feeding.
If she's not eager at first to eat her hay again either (grass is OK to start with if that's what you have available, but alfalfa or alfalfa pellets would be a really good choice now) it'd be a good idea to bring her some of her favorite browse... I feed Salal and wild huckleberry up here in the Northwest, both of which stay green all winter... In your area there must be something yummy, and non-toxic of course.

If you don't know her favorite, offer her a variety and let her choose. Keep in mind while treating your hypocalcemic doe that if she's been lying down for 3 or more days in this weakened condition you'll have to get her back up on her feet ASAP. Otherwise her leg muscles will lose strength fast and won't be able to support her if she tries to stand up on her own. There's also a chance that if she stays down for too long her knee joints will begin to 'ankylose' (freeze permanently in the bent position). This isn't reversible.

To avoid these problems you can make a 'sling' and attach it to a pulley fastened to an overhead beam in the barn. About every 2 hours crank her up in the sling so she can touch the ground comfortably with her feet, move around, and exercise her leg muscles, and then lower it again so she can rest for a while... Repeat the process, 2 hours up and 2 hours down, until her legs can support her weight again.
This usually takes only a few days, but in her pregnant condition she might take longer to get her strength back. If you want a picture of a sling I have one in my archives, at [email protected]

Prevention: You'd probably like to know how your doe got hypocalcemia in the first place, and how you can keep her from getting it again. Well, it's got to do with what you were feeding her before, during and right after she was bred.
If she was either under a year old or still being milked when you bred her, she should go right on getting the alfalfa and grain ration you were giving her to support her growth or milk production.
But if she was full grown and not in milk when bred, she should have been getting grass hay with no grain, or grass and some alfalfa with a little bit of grain at that time, and for the first 3 months of her pregnancy, because her body wasn't supporting any fetal growth yet.

Lots of owners don't realize that in those first 3 months all the fetuses do is develop their parts, and they're no bigger than newborn kittens. At the end of that 3rd month, though, the fully formed babies start to grow fast, and they keep that up for the entire last 2 months.
To provide for all this growth they need more and more calcium. To make that happen you'll have to start feeding a small amount of alfalfa along with the grass hay, and right along with the alfalfa, give her a handful of grain at each meal.

These amounts should be increased slowly over those next 2 months so that by the time she freshens she's getting all alfalfa, and about a cup of grain in the morning and a cup at night.
Once she's making milk she should get all the alfalfa she can eat, and depending on the amount she gives each time the grain should be increased so that she gets enough to help produce the milk but not make her fat.
A pound of grain is usually recommended for every 8 lbs (~ a gallon) of milk. I add alfalfa pellets to a doe's grain to keep her busy while I milk her out. As her milk production tapers off, both the alfalfa and the grain should be cut back, so that by the time she's dry she's only getting grass hay and no grain at all until the whole process begins again.

Cause: This hypocalcemia (calcium deficiency) problem that can show up any time in the last 2 months of the doe's pregnancy is easy to explain. It has to do with ratios. Most of us know that a ratio of 2 parts hydrogen to 1 part oxygen (H2:0) provides water. If that ratio isn't met, you don't have water. And people in copper-deficient areas might be aware that for copper to be available to goats the soil in which the feed is grown must contain a ratio of 10 parts copper to 1 part molybdenum (10:1).
Well, for calcium to be available to our does in late gestation or milk, a ratio of at least 2 parts calcium to 1 part phosphorus (2:1) is needed. When this ratio isn't met, calcium isn't available. So… If she doesn't get that 2:1 balance of (at least) 2 parts calcium (in the alfalfa) to (no more than) 1 part phosphorus (in the grain) in her diet, she won't have enough calcium to meet her needs and she'll become hypocalcemic. And it goes without saying that the more fetuses she is carrying, greater the potential for hypocalcemia becomes.

Let's review… Excepting for yearlings that still need calcium to grow, and does that are still in milk, when a doe is bred she should be eating grass hay with no grain, or grass and some alfalfa with a little bit of grain, because those tiny fetuses in her are in the early stage of development and not yet growing fast inside of her.

Unfortunately, many new goat owners (myself included, early on) start out feeding lots of grain as soon as the doe's bred, thinking that this will help her babies to grow big and healthy, when in fact it actually destroys the 2:1 balance needed to produce calcium, and puts her into a calcium-deficient state right off the bat!

In trying to do the right thing, the owner has taken the first step towards hypocalcemia, because when they reach the end of that 3rd month and have finished developing all their parts, those tiny fetuses just take off and start growing fast. And suddenly their mom is not just supporting her own needs, but also the needs of her fast growing babies, so she has to come up with lots of calcium she didn't require before!
Her amazing instinct tells her to listen to her body fast and cut back on the grain to meet the 2:1 ratio she needs to free up the calcium from the hay, or else! But unfortunately, when she quits eating her grain at this late stage so she can fix the calcium-deficiency problem, she loses her source of energy at a time when she needs it more than ever. So now, on top of being calcium deficient she also finds herself energy-deprived.
She starts to weaken fast, gets lethargic and wobbly, and goes down… And owners and consulting vets stand around scratching their heads, not knowing what led up to this. They'll probably offer her Nutridrench or propylene glycol to prevent the ketosis she's headed for, but they don't catch-on that the reason she keeps on getting weaker and weaker anyway is because even though they're replacing her lost energy the imbalanced early feeding program has left her too low on calcium to take care of her needs now.
So they fail to give her the missing calcium she must have for her own muscle tone as well as for fetal development. No calcium, no muscle tone, no heart pumping, dead goat.

This article is the result of my search through the various popular veterinary guidebooks, only to find that other than an occasional reference to the word 'hypocalcemia' itself, there is little else said about it. While it's a relatively easy-to-correct metabolic condition, oddly I can't find any description of what causes it, how to recognize it, how to treat it, or how to prevent it!
This despite the fact that it appears to be the most common dysfunction seen in does in late gestation and/or lactation, the only other one coming close to it being chlamydial abortion.

I've been trying hard to encourage the veterinary authors of these books to update their work to include this information, but progress is slow. While most goat management coverage in our current resource books is quite helpful, in this particular area I see deficiencies such as the following: (1) In the Merck Veterinary Manual In the 8th Edition on P.744, in the 'Pregnancy Toxemia in Ewes' section, the word, 'hypocalcemia' is mentioned only once, in a single sentence, under 'Diagnosis''.
It reads: "Hypocalcemia, uncomplicated by pregnancy toxemia, should always be considered for recumbent late-gestation sheep." Excellent! But that's the end of it! There's not a word on how to identify hypocalcemia OR how to treat it!
Then later, on P.1450, in the 'Disease Management Interaction: Goats' section, under 'Nutrition', we see, "A common problem is overfeeding grain to goats in late gestation." Perfect! They're right there at the threshold of hypocalcemia! But while they give lip service to the word 'hypocalcemia' on P.744, on P.1450 they're staring right at its cause and don't even know it.

They aren't connecting the dots between the danger of overfeeding grain to goats in late gestation, and the fact that it wrecks the necessary 2:1 ratio of calcium to phosphorus, making calcium unavailable to them.
Instead they state rather lamely, "Goats store fat preferentially in the abdominal cavity; this can lead to problems at parturition and to pregnancy toxemia."!
Then, in the ultimate irony, that's followed up by a second statement; "Pet wethers fed on substantial amounts of grain are prone to urinary calculi.
Reducing grain consumption… keeping the calcium to phosphorus to 2:1… will help." Good grief! They clearly have the tools, but don't know how to use them!

(Editor's note: As you will find later in this article, the well-known livestock nutritionist, Dr M.E. Ensminger, points out that both hypocalcemia and urinary calculi result from failure to maintain that 2:1 calcium to phosphorus balance in the diet.) (2) While the section on Goats' Dietary Needs in a popular goat management reference book called Goat Medicine, by Smith and Sherman, does a good job of pointing out the importance of a diet containing 2 parts calcium for each 1part phosphorus, the authors fail to apply that concept in other parts of the book where it's needed.
For example, in their 'Metabolic Disorders Appearing in Late Gestation' section they use the word 'hypocalcemia', but don't tell the reader (who often has no clue about a pregnant/ lactating goat's nutritional needs) that the way to avoid the mysterious hypocalcemia they've mentioned is to feed that same 2 parts calcium for every 1 part phosphorus diet that they already said was so important in their Goats' Dietary Needs section, thus freeing up the extra calcium she needs during gestation.
Instead, they follow up the hypocalcemia reference with a rhetorical comment about some sort of chemical imbalance within the hypocalcemic goat that makes calcium unavailable to her.
Oddly, in that same section on Metabolic Disorders there's yet another comment, this time that pregnant goats need "2 parts 'forage' to 1 part 'concentrate'", a misleading statement at best, and a recipe for disaster at worst, since many goat owners have only grass for forage, and grass has almost no calcium in it. (3) John Matthews, in his Diseases of the Goat, talks about 'hypocalcaemia', advising that it may appear in late pregnancy... AND in any stage of lactation… An important piece of information!
But he, too, misses the simple cause, a dietary imbalance that prevents the uptake of calcium from the feed. He relies instead on an unexplained "failure in the homeostatic mechanisms to meet the increased demand for calcium". But then in his discussion of 'Hypocalcaemia' he does redeem himself somewhat by saying that: "All recumbent or comatose goats should be treated as potentially hypocalcaemic and given calcium." Go, John Matthews!

So… Despite the importance these authors seem to place upon hypocalcemia as a potential diagnosis for late-gestation does that are down, none of them give us any clinical signs with which to identify it, nor any information on how to treat it, nor (equally as important) any suggestions on how to prevent it!

Yet as I previously noted, it's clearly the most common reason that does in late pregnancy or in milk 'go down'. Well, it's no wonder veterinarians in the field can't recognize hypocalcemia when they see it, when the authors of the reference books they use as guides don't either.
And the problem gets even worse when goat owners interpret statements made by veterinarians about the danger of feeding excessive grain (ex: Merck, P.1450, Nutrition) to mean that it would be best to feed NO grain, either to does in late gestation, or to wethers, because the 2:1 ratio of calcium to phosphorus is also lost when grain is removed from the diet, so feeding NO grain is just as harmful as feeding too much grain.

In my view, the reason these reference book authors use rhetoric, instead of providing information on diagnosis, treatment and cure to explain hypocalcemia, and the reason as well that the veterinarians in the field are comfortable relying solely on what they can find in the books to come up with diagnoses, is that neither the authors of those books nor the veterinarians who read them have sufficient nutritional background to know otherwise.
Sadly, an understanding of the principles of nutrition is not taught in schools of veterinary medicine. If it were required in order to earn a DVM I'm confident that this inability to properly diagnose hypocalcemia would quickly disappear.

Unfortunately for the goats (which after all are the focus of those reference books), when presented with a case of hypocalcemia, the total absence of information about its diagnosis, treatment and cure leaves the veterinarians nothing to work with excepting such off-the-mark diagnoses as Pregnancy Toxemia and Pregnancy Ketosis, for which diagnosis, prevention and cure ARE described in the books.
And even worse, when the vet's diagnosis is made and a savvy client asks if this could possibly be a calcium deficiency, the usual response will be, "This goat's problem has nothing to do with calcium." The predictable treatment regimen then will be: "Treat with propylene glycol for ketosis, and get the babies out fast to save the life of the doe." To accomplish that a C-section or, even more disastrous, a shot of Lutalyse to abort the doe, is suggested.
But that won't work because while the Lutalyse puts the doe into labor, without calcium the uterus has no muscle tone available to expel the fetuses.

(Editor's note: Ironically, the clinical signs of hypocalcemia are easy to spot, but are identified in the guide books as clinical signs of the diseases listed above instead, which is why the recommended treatment for those diseases commonly results in the death of the doe.)
Even after a veterinarian has declared pregnancy toxemia to be the culprit, on those occasions when I am consulted by an unsure owner and explain how I would treat the doe if it were mine, those owners have never lost either the doe or the kids in giving the 'down' doe CMPK instead of taking such drastic measures, and does treated to reverse hypocalcemia with CMPK routinely go on to freshen normally.

If my goat had this problem and I asked a veterinarian to help with it, I would expect that vet to work with me in treating the doe with CMPK before even considering anything as drastic as C-section or abortion! Many well-respected dairy goat nutritionists and veterinarians have mentioned hypocalcemia in their work over the years, but most haven't talked about what causes it, which is so important to its treatment.
Since livestock management is not their chosen field, maybe they assume that all dairy goat people instinctively know how to feed their pregnant stock correctly?

Following is an introduction to some of those whose contributions have helped us understand the dietary needs of our goats, and how to make corrections if these needs aren't being met: Dr M.E. Ensminger, the well-known livestock nutritionist whose work has helped many of our experts figure out what to put in livestock feeds, says in his 'bible' of livestock nutrition, Feeds & Nutrition - Complete, published in 1978, that Alfalfa (he calls it lucerne), a legume, "is high in calcium, protein, and carotene, and in many other minerals and vitamins", and adds, "legumes are excellent calcium sources, while grasses and silages tend to be substantially lower in calcium content".
Both bone growth and lactation (and muscle tone as well, BTW) require substantial quantities of these minerals. In his words, "If there is a severe imbalance of them during pregnancy and early lactation, 'milk fever' (hypocalcemia) may occur."

"Therefore, in order to prevent these problems, the ratio of calcium to phosphorus should be at least 2:1." (2 parts calcium: 1 part phosphorus.) (FYI: He also states: "In males an imbalance of calcium to phosphorus often leads to the development of urinary calculi.) Finally, for those of us who rely on grass hay to feed our goats, Dr Ensminger says that where additional calcium is needed, ground limestone is usually the mineral of choice.
But if the animals need both calcium and phosphorus the best choice for providing these 2 essential minerals is di-calcium phosphate (2 parts calcium: 1 part phosphorus). Adding support to Dr Ensminger's findings, mineral requirement charts in books on nutritional guidelines for humans state that a symptom of excess phosphorus intake is "decreased blood calcium", and a symptom of deficiency in phosphorus intake is "general weakness".

Both, of course, mean the same thing, since without calcium there is no muscle tone. This completely supports Dr Ensminger's findings that a severe imbalance either way of the 2 parts calcium to 1 part phosphorus requirement in the diet makes calcium unavailable, and the result of that is lack of muscle tone (ie: general weakness).

Another knowledgeable person with whom I've had the good fortune to come into contact was a veterinarian named Dr Robert A. Jackson, who lived in Southern California where I first began to raise dairy goats, and who was what you could call 'a goat vet's goat vet'. He and Alice Gaye Hall, a well-known dairy goat breeder/judge, often co-wrote dairy goat management articles. In one of them, printed in the July '82 Dairy Goat Guide and called 'What to Know about Medications', the readers are told that it's important for goat owners to keep calcium in their cupboards because goats often come down with "eclampsia, which is much like milk fever". (Just as others have, they referred to hypocalcemia as eclampsia.)

While they don't spell out why it happens, they do observe that a calcium deficiency (hypocalcemia) sometimes exists in the pregnant/lactating goat, and that the owner should be prepared to treat it when it shows up
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