Hypocalcemia in Goats

Episode 66
For the Love of Goats

Hypocalcemia in Goats

Hypocalcemia in goats, sometimes called milk fever, is one of the most misunderstood maladies in the goat world. This confusion stems from research done on cows, which does not apply to goats, but is still often referenced by many sources as if it does apply.

Today’s guest, Dr. Robert Van Saun of Pennsylvania State University, once again reminds us that goats are not little cows. We are talking about the causes of hypocalcemia in goats and how that compares to cows, as well as how to prevent it and the treatment.

Dr. Van Saun talks about intravenous, sub-q, and oral treatment, and how quickly we should expect each one to work.

We also discuss the relationship between hypocalcemia and pregnancy toxemia and how a diet to prevent one can also help to prevent the other.

Other episodes with Dr. Robert VanSaun

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Transcript – Hypocalcemia in Goats

Introduction 0:03
For the love of goats! We are talking about everything goat. Whether you’re a goat owner, a breeder, or just a fan of these wonderful creatures, we’ve got you covered. And now, here is Deborah Niemann.

Deborah Niemann 0:19
Hello, everyone, and welcome to today’s episode. This is going to be, I think, an episode that is going to really help clarify things for a lot of people. Because hypocalcemia in goats, also known as “milk fever,” is one of those things where you find a lot of contradictory information—and not just slightly contradictory, but 180-degrees contradictory.

Deborah Niemann 0:43
We are joined again by Dr. Van Saun from Pennsylvania State University. He’s a professor of veterinary science and also an extension veterinarian there. Thanks so much for joining us again today, Dr. Van Saun.

Robert Van Saun 0:55
You’re welcome. And glad to be here again.

Deborah Niemann 0:58
So, it’s a little weird. Some people may have heard the term “milk fever,” which is quite a misnomer, because the goat does not have a fever when they have this. “Hypocalcemia” is the more correct term, is that true?

Robert Van Saun 1:12
That is correct. “Milk fever” is an old but extremely common term, and it comes to us from dairy cattle. Back in the early 1900s, as we started to genetically select dairy cows for greater milk production, we started to get into some metabolic disease problems, of which the syndrome that we’ll talk about—hypocalcemia—is one. There is actually historical documents back in the early 1800s that talk about, you know, a disease process that would be, in today’s world, described as hypercalcemia. But they didn’t know what the problem was. Matter of fact, they thought it was a glucose deficiency originally. And from there, it wasn’t until, oh, I think the 1930s and into the 1940s, where they finally started to recognize that it was a calcium issue. And one of the first things, in dairy cows, that was done—and this may amuse a number of the listeners. I don’t know who figured this out, but they used to take a bicycle pump. Yes, a bicycle pump. And they pumped air into the mammary gland, into each quarter, and then taped it closed. And that allowed the cows to recover. And so, that’s where they finally figured out that it was loss of something in milk that was causing the disease process. And then, they ultimately determined it was calcium. And then that set in place lots and lots of research. I have students who choose milk fever in dairy cows as their research paper topic. And the first thing they come back to me about, they said, “Oh my gosh, there’s way too many articles to read on this.”

Robert Van Saun 3:17
So anyway, this gets us to our sheep and goats. And unfortunately, the hypercalcemic condition has just been termed “milk fever” because of, you know, the historical information with with dairy cows. In actuality, you know, hypocalcemia is more of a scientific term of what occurs. “Hypo” means “low.” “Calcia” is—or “calcis”—is “calcium.” And then “—emia” means “relative to blood.” So, this means low blood calcium concentrations. So, that’s essentially what occurs. This would be equivalent to what’s termed “pregnancy eclampsia.” So maybe some women in the audience might have had the experience of lactational eclampsia, and this is a situation where, during the lactation, the body is unable to maintain blood calcium, and they go calcium deficient, and that causes a wide range of symptoms, including muscle weakness and ultimately—potentially—even death. But that’s essentially what’s happening, is that the calcium is being lost from the blood and not being maintained.

Deborah Niemann 4:46
Okay. That’s really fascinating, especially the history of it. It’s very interesting.

Robert Van Saun 4:51
Yeah. Calcium… Once we discovered that calcium was the nutrient of concern in this disease process, then there was a lot of interest in exploring how calcium is regulated. And if the listeners will kind of bear with me here, I don’t want to get too scientific, but if you think about it, blood glucose is very tightly controlled when your hormones insulin and glucagon work together. Right? So, insulin decreases blood glucose, and glucagon increases blood glucose. And thereby, you can maintain a fairly stable blood glucose concentration, except for in disease conditions like diabetes, where either you don’t secrete insulin or your tissues become nonresponsive to the actions of insulin.

Robert Van Saun 5:47
Well, in the same way, calcium is very homeostatically regulated. There are two hormones. One comes from the thyroid gland, called “calcitonin.” And the other comes from the parathyroid gland, called “parathormone.” Parathormone responds to low blood calcium and enacts a number of activities in the body to increase the calcium concentration in blood. Calcitonin does exactly the opposite. If your calcium is high in the blood, then it causes reactions to decrease. We don’t want high blood calcium, because if we get that, it can precipitate into our blood vessels and harden them rather than allowing them to be elastic, or it can get into the mammary gland or muscle tissue or the lungs, and that could lead to severe mineralization of soft tissue, and then ultimately—potentially—death. And that mineralization can never be undone. That’s a one-way process.

Robert Van Saun 6:55
Now, many of you may also be thinking, “Well, wait a minute, we’re talking about calcium. What about vitamin D?” And that is a key player. Vitamin D is an important contributor to calcium homeostasis and works in concert with parathormone and calcitonin. So, when one of the hormones is active, like parathormone, parathormone turns vitamin D that flows in our blood into the active form of vitamin D. And it’s actually vitamin D that causes the increased absorption of calcium from the gut and mobilization of calcium from the bones. Calcitonin suppresses the active form of vitamin D, thus allowing calcium to be deposited in bones and to decrease calcium being absorbed. And so, vitamin D plays that critical role in providing the resources of calcium for parathormone and calcitonin to regulate and maintain a very tight window on blood calcium. For example, in goats, blood calcium ranges from about 8.5 to 11 milligrams per deciliter. That’s it. Anything below that is considered some form of hypocalcemia, and above that is hypercalcemia.

Deborah Niemann 8:23
Okay. So, when you said earlier that “there is a ton of research on this,” you meant in cows, right? Not goats.

Robert Van Saun 8:30
In dairy cows, right. And that’s the problem, is everything is related back to dairy cows, hence why they use the term “milk fever” as the, you know, the descriptor. This really… A common name for this in sheep is called “lambing sickness.” All right? It could be called “goat sickness,” too, or “kidding sickness.” But “eclampsia”—”pregnancy eclampsia”—would be a better term for this. “Eclampsia” just means “low, low calcium.”

Deborah Niemann 9:02
Okay. And so, that’s where it gets to be confusing, because there’s not a ton of research on hypocalcemia in goats. So a lot of people just automatically default and say, “Oh, well, this is what happens in cows, so that must be true in goats, too.” So, can you explain a little bit about that?

Robert Van Saun 9:19
Yes. So again, I want to emphasize: Goats are not small cows. All right? Goats are not small cows. And so, we can’t directly apply… There’s just so many things we could talk about in terms of the differences: the feeding behaviors of goats versus cows; the movement of material through the rumen system; the chewing behaviors; and so on and so forth. Now, the calcium homeostatic system—ie: the parathyroid, calcitonin, vitamin D—is exactly the same. It’s the same in all species. All right? But what is important is understanding the inputs and outputs, or outflows, of calcium from the system.

Robert Van Saun 10:07
So, if we think of calcium in the blood, that’s the major player. The calcium is in the blood in two forms. It is bound to the protein albumin, or it is in an ionized form—a calcium 2+. It’s the ionized form of calcium that performs all the biological functions. And the main functions of calcium, other than building our bones and teeth and those kinds of things, is muscle contraction. Calcium has to be in the muscle cells to cause the contraction of the fibers for muscle cells to function. That’s why, when animals are deficient in calcium, they’re paralyzed. They’re very weak. They can’t walk very well. They don’t pass urine. They don’t pass feces. They’re cold to the touch. It’s because all the muscles—and even the heart is affected. The heart doesn’t beat as well. So, a typical animal experiencing hypocalcemia, including a goat or sheep, will have a very rapid but very weak heart rate. So if you listen, it’ll sound very muffled. And so, that’s one of the classic things.

Robert Van Saun 11:34
So, there are two ways that calcium can get into the blood. We can absorb it from our gut, and that’s controlled by vitamin D—the active form of vitamin D—or we can mobilize it from our bones. Now, older animals, where their bones are basically more… They’re mature and more highly developed. They can’t mobilize their bones very well. This is why, in dairy cows, older animals are much more prone to hypocalcemia. I would state that that’s exactly the same in sheep and goats. The younger animals probably don’t get affected by this too much, as opposed to the older animals. The only other thing that can control or impact the input is the kidneys. The kidneys can reabsorb calcium that’s filtered out through, under the influence of vitamin D—the active form of vitamin D—and parathormone.

Robert Van Saun 12:39
So, the big question is: Why did we get this imbalance? Well, the problem is, is every day, the animal loses some calcium out through the gut, from cells or undigested material; it loses calcium out of the urine. But more importantly, calcium is lost to the bone, because the bone is constantly turning over, so there’s always calcium being put into the bone. But in the case of our production animals, significant calcium is lost in colostrum and in milk, or, in the case of sheep and goats, to the fetal bones—especially when they have multiples. And so this disease, pregnancy eclampsia, in sheep and goats, unlike what happens in dairy cows, it’s the loss of calcium in milk that causes the derangement in the calcium homeostatic system. Whereas in sheep and goats, it’s during pregnancy, and it’s due to an excess of loss of calcium that isn’t replaced fast enough to the fetal bones, especially in those animals that have multiples.

Deborah Niemann 13:58
Okay. That’s really interesting. So, if a goat is carrying, like, three or four kids, that actually takes more calcium than a cow that’s creating a single calf?

Robert Van Saun 14:13
Yep, yep. So the other aspect of this—and what makes it challenging for us with goats—is now we have sort of two distinct lines. We have our meat breed goats, and then we have our dairy breed goats. And again, there’s not much data. I mean, the meat breed goats, my experience to this point has been: They almost always, if they’re going to have eclampsia, it’s during pregnancy when they have multiple fetuses. I see that also in the dairy goats. But some of these high-producing does worry me that they could actually present with milk fever signs like a dairy cow. So the dairy goat… Again, I don’t have a lot of evidence on this. But I am concerned that it kind of can broach both aspects of hypocalcemia. So, that puts the dairy goat in a little more challenging situation.

Robert Van Saun 15:15
So where people get confused, then, is what to do to prevent it. And that confusion is based upon the fact that everybody is—or, not everybody. But almost everybody is applying the cow model to your goats.

Robert Van Saun 15:32
Exactly. So, let’s establish sort of the cow side of things. So, the early work that was done… Oh, boy. It was, like, in the 1950s and 60s through Ohio State. They recognized that it was calcium and phosphorus in the diet that was important. And so, they looked at calcium-phosphorus ratios in the diet and made sure that there was, like, a 2-to-1 ratio—similar to what we do with urinary calculi. But that didn’t help matters. So, we didn’t really decrease milk fever prevalence in our dairy cattle. Then, in the late 60s and into the 70s, what we found is if we feed a low-calcium diet during pregnancy—late pregnancy—it, for a lack of better word, jumpstarts the homeostatic system. It increases the parathyroid to release parathormone and activate vitamin D. So, it actually up-regulates the increased absorption efficiency of vitamin D from the gut and increased absorption of calcium from the gut through vitamin D and calcium released from the bone. So, that was the main thrust.

Robert Van Saun 16:57
Some work that was done at the University of Pennsylvania Veterinary School, you know, was seminal research work that really supported that, if we fed a low-calcium diet… And that’s the problem, is if we feed a low-calcium diet, we’re under-feeding the calcium to meet the fetal bone needs and that puts the sheep and goat into problems. So, we really do not want to follow that original dairy cow situation, because there is a much higher requirement per unit of fetal mass for sheep and goats with multiples for calcium than it is for a cow that has a single fetus. So, one thing I’ll say fairly definitively is: If you want to cause pregnancy eclampsia in sheep and goats, is feed a low-calcium diet.

Robert Van Saun 17:54
Now, let me add one more thing to that: Feeding a high-phosphorus diet can actually suppress the calcium homeostatic system. And so, you know, one of the things we need to be cautious of… We are worried about calcium-phosphorus ratios when we talk about urinary calculi in males. But in the pregnancy period, if we have a very tight calcium-phosphorus ratio, and the phosphorus is well above the requirement, phosphorus will interfere and prevent parathyroid hormone from being released. So, that means the animal can’t activate vitamin D and can’t increase the absorption. So, we’ve got to be cautious. In sheep and goats, I think, fundamental, we have to be cognizant of how much calcium we’re feeding. So, feeding some alfalfa—that might be heresy in the minds of some people—but feeding alfalfa with higher calcium is appropriate. This is not what we would do in dairy cows. So, this is one of those true distinctions between the dairy cow situation and our small ruminants situation. And then two, we want to be very cautious of the amount of phosphorus that’s going in.

Deborah Niemann 19:14
Okay. So, a diet that has alfalfa in it and either not too much grain or no grain.

Robert Van Saun 19:23
Well, you always want a little bit of grain. Otherwise, we’re going to put us into the situation of pregnancy toxemia that we talked about the last time, because remember: The other big issue that we’re worried about is providing glucose to support the fetuses. And glucose comes predominantly from consumption of grain through the process where you generate the bacteria, ferment the starch, producing the compound propionate, which then goes through the liver and becomes glucose. So, we always want to make sure we’ve got enough glucose in there, and grasses are higher in sugars, but alfalfa is not. Alfalfa has more pectins, which is a fiber, and that’s going to produce more butyrate in the rumen system.

Robert Van Saun 20:16
So, alfalfa is good for two reasons. One, it brings us more calcium; it’s highly digestible. And two, it’s higher in protein. And, you know, when we talked about pregnancy toxemia the last time, you know, I mentioned there is certainly some concern that we’ve got to maintain protein. And plus, there’s another whole topic that we can address at some point: Feeding higher levels of protein in the late pregnancy period will actually improve the immune response of the doe, so that it’ll drop the fecal egg count. And that could then minimize the parasite issues in the early post-kidding period.

Deborah Niemann 20:19
When I was working on Raising Goats Naturally, the vet professor who helped with the nutrition part of that said that she recommended that your hay be at least 50% alfalfa for the last six weeks of pregnancy. That more is fine, but you want at least 50% alfalfa. Does that sound about right? For somebody who’s looking for guidelines?

Robert Van Saun 21:23
I think that’s a pretty good guideline in terms of looking at the forage amount, and so on, that these animals would consume. The other nice thing about alfalfa: the fiber. Alfalfa stems are not highly digestible, which is not good, but they’re what we call very “buoyant,” so they move through the rumen very quickly, so they don’t kind of fill up the rumen like a grass would. And then we get that competition for intake. We can see a much-reduced intake on those does that are eating just straight grasses rather than a grass alfalfa or some alfalfa. And again, as we mentioned with pregnancy toxemia, when we have multiples in there, there’s only so much space in that abdomen for those girls to fit everything. And you don’t want a lot of fiber fill in the rumen, because it’s just going to constrain intake.

Deborah Niemann 22:24
Right. So for people that want to know more about pregnancy toxemia, we did that episode a couple weeks ago, so be sure to check that out.

Deborah Niemann 22:32
So it sounds like, in terms of, like, preventing both pregnancy toxemia and hypocalcemia, that feeding alfalfa at the end of pregnancy for goats is a really good idea.

Robert Van Saun 22:45
Yeah. If you’ve got good-quality alfalfa, that certainly goes a long way. Otherwise, you’re going to have to provide more mineral—a higher calcium mineral—to those animals.

Deborah Niemann 22:58
So, what exactly are the symptoms of hypocalcemia in goats? And at what point in pregnancy or after kidding would somebody expect to see those symptoms?

Robert Van Saun 23:10
Okay. So, with hypocalcemia during pregnancy, the first thing I’m going to start seeing is the animal’s not going to be very aggressive at the feed bunk, or coming up to feed. It’s going to be laying down a little bit more than usual. If you go up to the animal, it may feel cold to the touch. You know, so feel the ears and the skin; it might be a little bit colder to the touch. You may not see if an animal is… Well, she’ll be segregated from the rest of the does, you know, which is part of the signs of pregnancy toxemia that we talked about. She’ll be looking a little more depressed. All right? Head might be down and, you know, again, laying more. And then, if she’s been laying in an area for a period of time, you may notice that there’s no fecal matter and no wet spots behind her because, again, as I said earlier, calcium is required for all muscles to contract. And so if you don’t have enough calcium, your bladder can’t contract, the lower colon can’t contract, so the animal can’t expel urine or the fecal pellets. So… Now, if you’ve got a penlight—you know, a little flashlight-type thing—you can look at the animal, look into the eyes, and flash the light in the eyes, and hold it there. If the pupil does not constrict down—in other words, that opening in the colored membrane called the “iris” there—if that doesn’t constrict down, that’s a classic sign of hypocalcemia. Because again, the constrictor muscles that control that pupil opening can’t contract, and so you shine a light in their eyes, and their pupils don’t decrease.

Deborah Niemann 25:02
Okay. Oh, the other thing, too, that is kind of funny about hypocalcemia in goats is that the body temperature usually goes down, right?

Robert Van Saun 25:11
That’s correct. That’s correct.

Deborah Niemann 25:13
Which is why “milk fever” is such a misnomer. Because—

Robert Van Saun 25:16
Right, right

Deborah Niemann 25:17
—because actually, the fever goes down instead of up.

Robert Van Saun 25:20
Right. Body temperature goes down.

Deborah Niemann 25:22
Okay. And how far down would you expect it to go?

Robert Van Saun 25:26
Oh, you know, depending on the environmental conditions, if it… You know, during the cold weather, they can drop 2 to 3 degrees Fahrenheit. But normally, you know, anywhere from 1/2 to 1 degree Fahrenheit below what the normal, you know, temperature would be.

Deborah Niemann 25:44
And if you think you have a goat that has hypocalcemia, then what should you do in terms of treatment?

Robert Van Saun 25:50
Yeah. There’s a couple options. So, depending on how severe the hypocalcemia is… And the problem that we have is, we, at this point in time, have no method, no way—even a veterinarian has no way—to be able to take a blood sample and test it right there on the farm. So, this is different than what we talked about with pregnancy toxemia, where we have the meters. Now, some of this technology is in the works. So hopefully, if I remember correctly, I saw some advertisement for a new piece of equipment out of Japan that would measure blood calcium on the farm.

Robert Van Saun 26:33
But anyway: One, we could provide some oral calcium supplements, like there’s a compound called “calcium propionate;” it’s used in the bakery process. And we often use it as drench for pregnancy toxemia—or ketosis—in dairy cows, but it’s a readily available calcium source. So, that would be… We could use that. We could give that orally. But that assumes that there is still some motility to the gut. The other option is to administer calcium. And we need to be very cautious about this, because calcium can cause heart blockade and induced death very quickly. So, if one is careful and confident in their ability to monitor and put a needle into a vein, we would administer a 23% calcium solution. And for a sheep or goat, we would only administer somewhere between 30 and 60 milliliters. And this is in comparison to a cow, where we would give 500 milliliters. All right? So again, a huge difference.

Robert Van Saun 27:48
If you’re not confident in administering IV calcium, and the goat is in really tough shape, really depressed, then you probably should call a veterinarian and have them treat them. Otherwise, another option is to put that amount of calcium solution under the skin, you know, in front or behind the shoulders. Now what I would do, though, is—if you do want to try and do that—find a calcium solution that does not have dextrose in it. So, you just want a 23% calcium borogluconate solution with no dextrose. Why we don’t want dextrose is, when you put dextrose—which is basically sugar water. If you put that under the skin, there’s a high risk that that could ultimately abscess, and then you’re going to have this draining tract and everything. So, you don’t need—the goat doesn’t need—any more problems. But again, the neat thing about hypocalcemia is, if you treat them, it’s like a miracle cure; they just, like, get up and walk away and don’t even look back. But we’ve just got to make sure that we don’t overdo it, because this is an easy one to overdo.

Deborah Niemann 29:08
Right. And the treatment, if it’s successful… Like, if that’s what you’re dealing with, it should be really fast. Like, we’re talking minutes?

Robert Van Saun 29:17
Yes. If you treat intravenously, the response should be within 5 to 20 minutes, or even earlier. If you give it subQ it might take 30 to 40 minutes.

Deborah Niemann 29:30
Okay. All right. That’s one of the things I think is so incredibly important for people to know, because I actually… I never had a case of hypocalcemia on my farm, but I thought I did one time, because the doe had given birth the day before. It was a LaMancha. She’d had triplets. I walked in there, and she was laying in the corner; her kids were jumping all over her, screaming and bopping her, and she was just oblivious to them.

Robert Van Saun 29:57
Yeah.

Deborah Niemann 29:58
Her udder was, like, floppy and ice-cold, and her body temperature was low. And I was like, “Oh my gosh, she’s got hypocalcemia.” And I couldn’t leave. And so I called somebody and had them pick some up for me at the store and bring it to me, because I had another goat that was, like, kind of in labor. And so I didn’t… And it was cold. I didn’t want to leave. And I just did not appreciate how fast she should have responded if that was it, because she didn’t respond. I gave her the injectable under the skin, and she didn’t respond. And I gave her another injection a few hours later; she didn’t respond. And then she died. And I was like, “Oh my gosh, why did she die?” I sent her in for a necropsy, and they—it was, like, crazy. They said she had both pneumonia and mastitis, either of which could have killed her.

Robert Van Saun 30:48
Right. Right. I would have figured something like that. That she probably had a pretty nasty mastitis.

Deborah Niemann 30:55
Yeah. And I just… That’s just so weird, because you think “mastitis,” “Oh, the udder is gonna be big and hard and hot—

Robert Van Saun 31:00
Not always. Yeah.

Deborah Niemann 31:02
—and it wasn’t. It was cold and floppy. And so—

Robert Van Saun 31:07
Yeah. That could have been almost the beginnings of the gangrenous-type mastitis, where it started to change color and stuff.

Deborah Niemann 31:15
Yeah. And had I realized, like, “Okay, it’s been an hour, she did not respond to this. Something else is wrong. She needs to see a vet right away.”

Robert Van Saun 31:24
Yeah. So we talked about, we don’t want to use the dairy cow preventative process of feeding low calcium in the prepartum or the late gestation diet. I get a lot of questions from even some very, very experienced goat producers about this concept of what’s called “dietary cation-anion difference,” or DCAD. All right? So, some work that was done in the… Oh, the mid-80s, and continued through the 90s, in dairy cows, was when we recognized that it wasn’t practical to feed a low-calcium diet for dairy cows. And it wasn’t as successful as what the research sort of suggested it would be. We stumbled on this concept of, if we acidify the animal—and so what we’re talking about is manipulating the acid-base balance of the animal’s body. It turns out calcium is absorbed more efficiently in an acidic environment. And the production or synthesis of active vitamin D is more efficient in a slightly acidic environment.

Robert Van Saun 32:54
And so, some really classic research that was done out at Iowa State in the… It was the mid 90s, where they fed diets with higher potassium or higher sodium, they could induce milk fever in dairy cows like crazy. And so, sodium and potassium both have a positive charge, so these are called cations. And they, when they get absorbed, they shift the pH to what we call more “alkaline.” So, above-neutral. Negatively charged compounds, like chloride and sulfur, they induce acidotic state. And so, now what we do in dairy cattle rations is we calculate the balance between the cations—the major cations—sodium and potassium, and the major anions, the chlorides and the sulphurs. And that gives us this dietary cation-anion balance. If we can get that diet—DCAD, as it’s called—down negative, or at least to 0, we seem to increase the capabilities of the homeostatic system and improve and reduce milk fever incidents in our dairy cows.

Robert Van Saun 34:24
So, people who work with high-producing dairy goats are, again, concerned—again, extrapolating from the dairy cow situation—that maybe dairy goats get into this subclinical or clinical hypocalcemia right after kidding. And so, they’ve thought about feeding these DCAD—these low-DCAD—diets prior to kidding, through. Now, this concept of DCAD is the whole basis of why we use ammonium chloride to prevent urinary calculi in males, because you’re adding that chloride to acidify, and that prevents the struvite crystal from forming. We just don’t know if this is necessary in dairy goats.

Robert Van Saun 35:19
This is, to me, the truly unknown situation. And I’m hoping… I have some collaborations with some large dairy farms here in the U.S.—dairy goat farms. And we’re going to start looking at this. We’re going to be taking blood samples, and maybe explore the possibility of using DCAD diets, and seeing if this doesn’t improve, or at least establish if we do have a similar situation in dairy goats, what we call “subclinical hypocalcemia.” So, they’re not down and out. But they’re just not eating well. They’re not performing well. They’re slow coming up in milk, and things like that, you know. So those are what we call the “droopy” cows. So, is there a “droopy” goat syndrome in the early post-kidding period that might be due to marginal calcium deficiency? So, we’re talking about calcium blood concentrations around 7, 7.5, you know, somewhere in that range. Just below normal.

Deborah Niemann 36:27
Okay. That sounds really fascinating. I’m so excited that you’re working on that research, because we certainly need more goat research on these nutrition topics.

Deborah Niemann 36:37
One thing I want to address is something that gets thrown around the internet a lot, and I would like for you to address this, and that is the use of Tums—the human drug Tums—in preventing and treating hypocalcemia in goats. Like, should people be giving their goats Tums?

Robert Van Saun 36:58
Actually, I’ve heard that from some of my veterinary colleagues—that are well-established sheep and goat veterinarians. Tums, basically, is a calcium carbonate source. And that calcium is quite readily available. So, when I talked about using calcium propionate as a drench, Tums could be used. Now, I’d have to go back and look at how much calcium is in Tums, and how many Tums might be necessary. And that might be prohibitive, but—

Deborah Niemann 37:37
It’s not many. It’s 500 milligrams.

Robert Van Saun 37:40
Yeah, so 500 milligrams is half a gram. And these girls are probably losing 4 to 5 grams to the fetuses a day, and they have another, probably, 8 grams in their blood. So yeah, half a gram isn’t… I mean, you’d have to give it a whole roll of Tums or something. So that may not be the best option. But the concept is sound in terms of a calcium… You know, if we can increase the soluble calcium in the gut, it will drive calcium across the gut wall and increase absorption. And this is what we’ve done with using soluble calcium solutions, like calcium chloride or calcium propionate. I wouldn’t recommend calcium chloride in sheep and goats, because it’s pretty caustic. You can actually cause lesions in the esophagus and in the pharynx—you know, the back of the throat. It’s very acidic. But the calcium propionate is good.

Robert Van Saun 38:48
We usually give about 250 grams of calcium propionate to a dairy cow. So, we’re probably only looking at, at best, 25 grams of calcium propionate, you know, mixed in some water—it’s very water-soluble—and you could either drench them with it or tube it into their their rumen or something like that. What you’re going to do is, you’re going to increase that soluble calcium concentration in the lumen of the gut, and that’s going to drive the calcium across the the gut wall through the between cell regions of the gut. This is a common practice that we use. There are commercial calcium boluses that we use in dairy cows; I guess you could use those, but they’re too big to administer to a sheep or a goat. You’d have to kind of break them apart. But giving that would be appropriate. But it’s a lot easier to let the goat eat some alfalfa hay.

Deborah Niemann 39:50
Yeah, exactly. When people have asked me about Tums, I’ve compared it to, like, the oral calcium drenches that are on the market. So, I also want to ask you about those. Like, one of them that is made specifically for goats has 3.75 grams of calcium per ounce, and they recommend a 1-ounce dosage. So, that’s why I always tell people, I’m like, “Well, you’d have to give them, like, almost eight Tums to be as much calcium as an ounce of this drench.”

Robert Van Saun 40:17
Yeah. So, 3.7 grams would be a pretty good dosage of calcium, so they’re probably right on the mark. I would think between 3 and 5 grams. So, if we have a half a gram in Tums, you’d have to be given 10 Tums, you know, to get that effect.

Deborah Niemann 40:36
Yeah. So, that’s a lot. It’s like, definitely…

Robert Van Saun 40:38
Yeah.

Deborah Niemann 40:39
The people who are like, “Oh, give them a Tums,” it’s like, that’s really not gonna help. That’s not enough calcium.

Deborah Niemann 40:45
So, if somebody is in a situation where they think their goat may have this, and they don’t have the injectable available, how do the orals work? And how soon should you expect to see them respond positively to an oral drench, if that’s the problem?

Robert Van Saun 41:06
Yeah. So with an oral drench, the way that works is you’re increasing the soluble calcium in the lumen of the intestine. And because of that concentration gradient, the calcium will move between the cells—what we call a “paracellular-type transport”—and we get that absorption. In terms of time, this takes a few hours.

Deborah Niemann 41:37
All right. So, if a goat really is in trouble, it’s better to do something injectable or get them to the vet.

Robert Van Saun 41:43
Yeah. Now we do see… I don’t see it as much in our sheep and goats. We certainly see what we call “relapses” of milk fever in dairy cows quite a bit. And again, it’s just because when we give the big IV dose, of course, when the calcium goes up high in serum, that means parathormone is suppressed and calcitonin kicks in. And so then, you know, once that calcium in the blood is redistributed, the homeostatic system is blunted, and so they’ll relapse again. I’ve not heard so much, but I hear, you know, from some people that they’ve seen sheep and goats that do relapse. And I did have one case, when I was out in Oregon, of a sheep flock that was running into these problems. And it was mostly because the pasture they were on had very low calcium and very high phosphorus. And we treated with IV calcium; she relapsed the next day, we gave her IV calcium again, and she was fine after that. So, you may have to treat—especially if you treat IV—you may have to treat them a second time.

Deborah Niemann 42:59
Okay. And then, I’ve also seen some people say that, like, a goat doesn’t necessarily have to be, like, right around that periparturient period to get hypocalcemia. Up until, like, how far after kidding would you say, “Okay, that’s not hypocalcemia. Something else is going on”?

Robert Van Saun 43:20
Well, you know, again, more commonly, it’s going to occur prior to kidding. And that can be weeks prior to kidding, because of the calcium loss to the bones. In the postpartum period, you would expect most of this to occur within the first 72 hours. But that being said, if your lactation diet is not properly balanced for calcium, as these does hit peak milk, they can actually go into lactational eclampsia. And we see this in many species, even in human species. Women that are lactating, they don’t take in enough calcium, and they’re losing so much calcium through their milk that they actually get into a hypocalcemia condition at peak milk production.

Deborah Niemann 44:13
Wow, that is fascinating.

Deborah Niemann 44:15
All right, well this has been really educational today, and I know you’ve answered a ton of questions for people who’ve been really confused about this, and I think did a great job of explaining why people see so much different information out there, which I think is really important for people to understand. Is there anything else you wanted to add?

Robert Van Saun 44:36
I think we’ve really covered in detail quite a bit of that… I guess one last point is in the National Research Council recommendations for nutrient requirements, which we use as our guideline. When you compare calcium requirements for sheep and goats, goats have a much higher calcium requirement than sheep. So, you know, again, I think in our goats, we really need to be aware of the calcium concentration in our diets and making sure our phosphorus isn’t too high.

Deborah Niemann 45:12
That’s great. Thank you so much for joining us today.

Robert Van Saun 45:15
You’re welcome.

Deborah Niemann 45:17
And that’s it for today’s show. If you haven’t already done so, be sure to hit the “subscribe” button so that you don’t miss any episodes. To see show notes, you can always visit ForTheLoveOfGoats.com, and you can follow us on Facebook at Facebook.com/LoveGoatsPodcast. See you again next time. Bye for now!

hypocalcemia in goats

9 thoughts on “Hypocalcemia in Goats”

  1. Calcium chloride is the main ingredient in the drench I purchased.
    Since Dr Van Saun doesn’t recommend using this in goats can you recommend a product which uses calcium propionate?

    Reply
  2. Can an IV in a hypocalcemic goat dilute blood calcium, precipitating death? My friend’s post-partum doe collapsed and died very shortly after receiving an IV.

    Reply
    • I’m not sure I understand your question. If she had hypocalcemia, and she received an IV, it should have had calcium in it. As Dr. VanSaun talks about in this episode, goats have the fastest improvement when given intravenous calcium. There would be no reason to just give her an IV with no calcium in it.

      Reply
  3. Thank you for this podcast! We bought a goat who has had this in the past, and she’s due next weekend. I had trouble finding much info on this in goats. So appreciated!

    Reply

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