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Floppy Kid Syndrome
SymptomsVeterinary info, very much on target regarding the symptoms, notes the following: Kids are born healthy, and up bouncing around… But then suddenly, starting anywhere from 3 to 10 days after birth, they're down and showing signs of depression, weakness, and flaccid paralysis. Affected kids can still swallow, but can’t use their tongues to suckle. Rectal temperature is normal... There are no advance warning signs. The one obvious clinical sign is distention of the abdomen. If blood chemistry is done, an unexplainable acidosis is apparent.
TreatmentThe veterinary community is pretty much in accord on this issue, advising the owner to treat ASAP with oral Pepto Bismol, along with either oral or subcutaneous sodium bicarbonate solution (very hard to find!) or, as an alternative, tubing with baking soda diluted in water. This is to counteract what they currently view as the unexplainable acidosis that’s present in FKS kids.
(These treatments are ‘as needed’, dependent upon the extent of the acidosis. If mild, only 1 treatment may be sufficient. If more severe, it may take 2 or more treatments to bring the kid back to normal.)
(A personal addendum: I urge the owner to add a preventative dose of C&D antitoxin to the FKS treatment regimen, because the stopped-up gut, which naturally contains Clostridium perfringens, is a perfect medium for development of enterotoxemia. If preventative measures are not taken, the kid might die in great pain despite the Pepto Bismol and baking soda treatment.)
CauseThe veterinary community hasn’t been able to come to any real accord as to what actually causes Floppy Kid Syndrome in the first place, thus presently no official veterinary consensus exists as to what, if any, measures can be taken to prevent it from happening.
However, definitive answers to mysteries such as this can and often do come from outside the veterinary community… And an observant owner’s day-to-day hands-on management can often uncover clues that explain the otherwise ‘unexplainable’ but are simply not available to most veterinarians, who lack that opportunity for ongoing hands-on management and observation…
As a professional educator with a strong background in nutrition, and with 35 years’ experience in daily hands-on management of my own dairy goats, a penchant for researching, analyzing, and testing out new ideas and a strong belief in “learning by doing”, I have indeed gained insight and picked up clues as to what causes Floppy Kid Syndrome (FKS).
My own experience tells me that the cause of FKS lies with the diet fed to the dam in late gestation, a diet recommended not by livestock nutritionists (in whose bailiwick such authority should lie), but rather by the veterinary profession (which is largely made up of veterinarians with no nutritional background whatsoever to draw upon). This veterinary-recommended late-gestation diet is totally contrary to the fundamental principles of nutrition.
The fact is, in late-gestation the babies’ rapid growth puts a huge drain on the calcium in the mother’s system. The more fetuses there are, the more calcium the mother will need. To make calcium available in sufficient quantity to meet the needs of both the mother and the fetuses, the mother’s diet must contain a basic nutritional formula that provides at least 2 parts of calcium-food (alfalfa is generally the only available* forage out there that contains lots of calcium) to every 1 part of phosphorus-food (grains are loaded with phosphorus). If that need is not met in the mother’s feeding program during that last stage of gestation she’ll go into hypocalcemia (calcium deficiency). Calcium is as important for the mother’s own body function as it is for the babies’ development, because among other things it’s essential for muscle tone, and the uterus is a muscle. The more fetuses she’s carrying, the more hypocalcemic she’ll be and the less muscle tone the uterus will have. Thus birthing will be slow and inefficient and may require assistance.
I should note that a doe’s hypocalcemic condition doesn’t always result in FKS kids. Two aspects must be considered. One is the severity of the nutritional deficiency causing the hypocalcemia, and the other is the number of fetuses draining the available calcium from the mother.
Where the hypocalcemia is severe, AND there are 3 or more fetuses draining the mother of her available calcium, unless this condition is treated and reversed quickly by an observant caregiver, both the mother and the fetuses will die.
Where (a) the hypocalcemia is severe, but there are only one or two fetuses, or (b) the hypocalcemia is mild but there are 3 or more fetuses, the doe will probably go into labor uneventfully but it will be slow, the afterbirth will be retained, and the potential for FKS in the babies will be high.
Where the hypocalcemia is mild and there are only one or two fetuses, while the labor won’t be as efficient as it could be, barring ‘mechanical’ problems (ie: kids presented wrong) the likelihood of producing FKS babies is relatively small.
Interestingly, in discussing FKS a number of academically oriented veterinarians (the ones who influence what’s written in the veterinary textbooks) do inadvertently reveal clues as to the role an incorrect diet plays in compromising the birth, thus laying the groundwork for FKS, but because they lack background in nutrition they’re unable to make a connection between the two.
This is illustrated by three random examples below. All of them, BTW, unknowingly support my understanding that the mother’s nutritional deficiency in late gestation is the direct cause of FKS.
# 1: This contribution is excerpted from notes taken at a seminar on FKS given by Kathy Bretzlaff DVM, Small Ruminant Specialist at Texas A&M University's College of Veterinary Medicine, for owners of Boers and other meat goats: She says, ”All producers who brought affected kids to the San Angelo research station had improved nutrition of the nannies this year as compared to previous years, either with corn or concentrate feed, or by putting in irrigated/improved pastures some time before parturition.¹
(My translation: The owners producing these FKS kids had increased the mothers’ grain, thus increasing phosphorus intake, and had also put them on grass hay, which contains almost NO calcium, in late gestation.¹ Thus the dams were in a hypocalcemic state when the kids were born. She had a good clue there, but didn’t know how to use it!)
Dr Bretzlaff ended the talk with a ‘guesstimate’ (a rather lame one in my view) that the cause of the FKS must have been that some started kidding in enclosed pens, giving kids the opportunity to suckle more often and consume more milk, therefore the condition was probably the result of over-consumption of milk, indicating that microorganisms in the gastrointestinal tract lead to changes in digestive tract acidity.”
# 2: The 2nd contribution, from an article on FKS by Joan Dean Rowe DVM, professor at the Univ of California Veterinary Teaching Hospital, is: “In a review of case histories from multiple herds, no association was found between treatment with a variety of vitamin/mineral supplements and/or antibiotics and clinical response. Clostridium botulinum, E. Coli, and Caprine herpes virus have been proposed as candidate etiologic agents, however these agents have not been definitively proven or excluded as potential causative agents. Because the etiologic (causative) agent is not known, aside from correction of electrolyte imbalance and supportive care, no preventive or therapeutic treatments can be specifically recommended. The reversibility of this syndrome is intriguing and suggests a transient initiating insult (aka some unknown factor set the whole process in motion).”
(My translation: Because we in the veterinary community have no understanding of nutrition, while we know what to do to fix FKS we haven’t a clue as to what causes it, thus we have no clue either as to how to prevent it. But we’re pretty sure that SOMETHING that’s preventable is the cause.)
In my view Dr Rowe’s observation is quite rational, as it rules out potential culprits but doesn’t try to ‘guesstimate’, nor to draw conclusions, as to the real cause of FKS, forthrightly stating that the veterinary at large has not yet solved the mystery.
# 3: I find this 3rd contribution particularly interesting since the work was actually done with Fading Puppy Syndrome (FPS), yet the findings are parallel to those found in the research done on Floppy Kid Syndrome (FKS), to the degree that I’m convinced they have a common cause. It comes from notes taken at a veterinary seminar put on by Jacob Mosier DVM, a well respected small animal veterinarian at Kansas State University College of Veterinary Medicine. He says: “At birth a newborn puppy should have a pH level of 7.4. A puppy can be hung up in the birth canal for too long or the bitch might not remove the sac, causing delayed breathing. We need to be sure it breathes fairly soon because the longer it doesn’t, the more its blood pH level drops, the more acidotic it becomes. During the time it’s still wet (about 20 minutes), the pH drops to about 7.1. If it drops to 6.6 the heart will stop. Despite the delay in the birth process, once revived and breathing the FPS pups appear healthy and strong. But around the 36th to 72nd hour³ they begin to fade and lose vigor, and the tongue is pale. By the 96th hour they become flaccid and die.”
(My translation: Because the hypocalcemic bitch lacks sufficient muscle tone to expel and tend to the fetuses efficiently, they take longer to get out of her and breathe on their own. Lacking oxygen, their pH drops, causing acidosis. In my view this explanation of why FPS occurs in puppies explains why we need sodium bicarbonate to reverse acidosis in FKS kids.)
Dr Mosier goes on to ‘guesstimate’ the possibility that some sort of uterine infection harbored by the mother might set up the conditions that lead to FPS (aka FKS in goats). Similar conjecture has been made by other veterinarians, but here’s no concrete evidence to support it.
Prevention: Observations made in the three contributions above completely support my own understanding of what causes FKS, and of the changes that must be made to prevent it. As I note in the articles I’ve written on Hypocalcemia, its prevention requires that during the first 3 months of gestation the bred doe should be on a “non-working” ² diet of grass or timothy hay. But as she enters her 4th month of gestation when the fetuses really start growing fast, she should be switched to a “working diet”² that will give her the needed calcium-foods and phosphorus-foods in a ratio that provides her with at least 2 parts of calcium to every 1 part of phosphorus. This is critical, because if a doe in late gestation eats plenty of alfalfa, but NO grain, there’ll be a phosphorus deficiency. And if she eats straight grass hay and lots of grain, there’ll be a calcium deficiency. Either way the nutritional balance is off. Only a doe that isn’t ‘working’ (growing, pregnant or lactating) can survive on a diet like that. BTW: the bonus to the diet I recommend is that it doesn’t just prevent FKS…It also provides an ideal level of nutrition in late gestation!
Addendum: At the same time that I started raising dairy goats, I also began raising Australian Shepherd dogs. Early on, whelping my Aussie bitches commonly took anywhere from 12 to 24 hours. Weak and fading puppies were not unusual. After discovering what caused hypocalcemia in my dairy goats I transferred that information over to my dog breeding experience as well, and as soon as I began providing the bitches with a hypocalcemia-prevention diet in late gestation (contrary to the advice given in the canine veterinary books) I discovered that whelping time for the same sized litters as before was reduced to 3½ to 4 hours, and the neonate puppies all came out vigorous and healthy. End.
* Clover is equally as rich in calcium as is alfalfa, but it doesn’t bale well, thus it is harder to find. Kelp is also very rich in calcium, and other desirable minerals as well, but difficulty in obtaining large quantities of it makes it less accessible to goat owners.
¹ It’s been subsequently noted that the meat goat breeds have had a higher than average number of FKS kids among their populations.
² A “working diet” is fed to goats that are growing, in late gestation, lactating, or (in the case of bucks) in breeding season. A “non-working” diet, then, is a subsistence ration that’s fed to healthy goats that are neither growing, in late gestation, lactating, nor (in the case of bucks) breeding.
³ Puppies are less mature than kids when born, thus the problem shows up much faster.
(While I urge you to share this information with other individual goat owners, please do not alter nor reproduce the article, nor any part thereof, for publication without my specific permission.)
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|Started By||Thread Subject||Replies||Last Post|
|CarleneWheeler||hypocalcimia||0||Aug 2 2011, 6:55 PM EDT by CarleneWheeler|
Thread started: Aug 2 2011, 6:55 PM EDT Watch
I really like your article and have a question for you. I had my first indications of Hypocalcimia this year and handled it with CMPK. The consensus that I have come to is that it arose from
my feeding hay from fertilized fields which I have never had this hay before. Usually I have no problems and just keep the grain light until about two weeks before kidding. Can you relate to this?
Any other suggestions for next spring ?
|GoogooLadu||Floppy Kid Syndrome||0||Mar 15 2009, 11:34 PM EDT by GoogooLadu|
Thread started: Mar 15 2009, 11:34 PM EDT Watch
Dear Goat Guru,
I want to thank you for going through the Floppy Kid Syndrome.
I believe you are accurate generally, but in the mountains where
calcium is short in the goats diet, I believe I am seeing it not only
at the first 36 hours, but in older goats with multiple births
I am seeing it at birth, and the kids never come out of it.
I am up now with a kid that is actually growing,
has good head and tongue movement, but has
never developed muscle tone in the legs. And
he is going on one week.
Thanks for your help.
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