Inge1104 hat geschrieben:Hallo!
Bigi hat heute außer ein paar Karottenstückchen kaum was gefressen; sie mag weder Kraftfutter noch Heu, und auch trockenes Brot frisst sie nur aus der Hand. die arme Ziege sieht richtig dürr aus :(
@ Johanna: ich werde jetzt mal Apfelsaft in ihr Wasser schütten und hoffe, dass sie dann mal wieder säuft.
hallo inge
wenn deine ziege nicht frisst und so mitgenommen aussieht ist das ein sehr ernster zustand. trinkt sie noch?
wieviel kraft futter hast du ihr gegeben am anfang der schwangerschaft?
lass den TA kommne und frag ihn ob es ketosis sein koente?
druck dir doch diesen article aus und geb ihm den zum lesen. warte nicht damit sonst koenntest du deine ziege verlieren.
KETOSIS: What is it Actually, and How Does it Happen?
(Please feel free to give a copy of this article to your veterinarian if you would like to do so)
Ketosis is a word that gets bandied about a lot, indiscriminately in my view, and it is incorrectly said to be the primary cause of a number of ailments. One that comes to mind, because I see it mentioned often, is "Pregnancy Ketosis". There is no such thing! There is pregnancy, which is one condition, and there is ketosis, which is an entirely separate condition. Ketosis can develop as a secondary condition under some circumstances during pregnancy or lactation, but it isn’t limited to pregnancy or to lactation, and it can show up at any stage in the life of a goat. (BTW: ketosis happens to people, too.)
The word itself is not well understood, so I’ll try to explain it: In technical terms, it’s a condition brought on by a metabolic imbalance. In scientific terms it’s defined as an accumulation of excessive amounts of ketone bodies in body tissues and fluids. 'Ketone bodies' are the metabolic substances known as acetoacetic acid and beta-hydroxybutyric acid. Acetone, which puts off the peculiar odor associated with Ketosis, comes from acetoacetic acid. These substances are all normal metabolic products of 'lipid' within the liver. When they become severely imbalanced as the result of ketosis, the liver will fail.
Cause: By its very nature, Ketosis has to be a secondary condition, because it’s the direct result of a process that starts when the animal, for whatever reason, stops eating. Why the animal stopped eating is the primary factor that must be addressed and corrected. And that must be dealt with quickly, because when it stops eating, the lack of an external energy source forces it to use its own reserves to provide energy. These reserves are in the form of fatty tissue. In the words of Dr WC Allenstein, DVM, a cow vet that wrote for Hoard's Dairyman for many years, "When this fat utilization occurs, free fatty acids are released into the blood stream and are used by the liver for energy. If this occurs at too fast a rate, the liver is bombarded with too many fatty acids, and there is an increase in ketone bodies released into the system. At a certain level the classic symptom of acetone odor on the breath and in milk [if the animal is lactating] will occur... The ketone bodies formed by incomplete fat metabolism by the liver create these symptoms." He goes on to say: "Today we know that anything that disturbs the body - other diseases, missed feedings, conditions disturbing feed intake, will create ketosis."
Lori Ward, then a student in Dairy Sciences at the U of Wisconsin, noted in an article that when the animal is forced, by lack of an external energy source, to turn to its own body for sustenance, "The body fat is mobilized to supply needed energy. The mobilized fat is processed in the liver, and it tends to accumulate. In most fatal cases the post mortem findings reveal a fatty liver. During fat mobilization, ketone bodies (one of which produces acetone) are produced and circulated in the blood, hence the names ketosis or acetonemia." Lori notes that most of the accepted ketosis treatments attempt to raise blood glucose in some manner. This provides a quick energy source for the victim, ending its need to live on its own fat reserves to survive.
A classic example of how ketosis gets involved (and often is the only disorder that gets recognized and treated, the end result being the loss of the victim’s life) is found in an article I wrote on Hypocalcemia. When a pregnant doe is being fed a dangerously imbalanced ration and stops eating a large part of that ration to instinctively try to correct the imbalance, the loss of this external energy source makes her turn to her own body's resources for survival. Since the babies are still growing in her it is very important to fix the original nutritional imbalance, which in this case is a diet-induced calcium deficiency. The fetuses inside of her are draining her of her own calcium, because of which she loses her muscle tone. Without calcium she becomes very weak. So she has weakened muscles, including the heart muscle, and at the same time is living on her own body reserves because she has stopped eating (and soon is too weak to eat) her imbalanced ration. When a pregnant doe becomes hypocalcemic and is mis-diagnosed by a vet who doesn't understand the dynamics involved, he fails to give her calcium replacement therapy at the time he is reversing the ketosis with energy replacement substances such as propylene glycol or Nutridrench. The result is a drained and weakened system despite the treatment for ketosis, and she inevitably dies either of 'unexplained' causes, or of what the vet labels 'milk fever', or 'pregnancy toxemia', or 'pregnancy ketosis', or 'parturient paresis', all of which are mis-nomers. Then if he does a necropsy he will generally label the cause of death as 'liver failure'. I don’t agree that liver failure is the actual 'cause' of death. I see it as the 'result' of the animal's not having been diagnosed and treated for both the primary cause, hypocalcemia, and the secondary cause, ketosis, because of which she dies. The liver failure, then, is not the cause of death, but simply the end result. Ketosis is the secondary condition involved. The survival of the animal is dependent upon the discovery and correction of the primary condition.