babsbag
Herd Master
@Sweetened I never thought about Ketosis. So here is a good read.
http://www.acga.org.au/goatnotes/D010H.php
The clinical evidence of ketosis usually appears during the period leading up to peak lactation (six to eight weeks after kidding).
Sub-clinical form — Many high producing dairy animals are on the borderline for ketosis. Intermittent periods of indigestion may take place with excessive amounts of highly digestible food, which may result in high levels of volatile fatty acids. Excessive acidity is liable to cause a stand-still of rumen activity and a chain of metabolic events resulting in excessive fat breakdown and ketosis. In this mild form, does will have irregular milk production and days of inactivity.
Clinical form — In the more severe form, the clinical findings include:
Diagnosis is generally based on the doe's history (time of kidding) and the clinical findings. However, the clinical signs can be confused with hypocalcaemia (milk fever), enterotoxaemia (pulpy kidney), bloat, impaction, reticulitis and nephritis.
The presence of ketones can be established by using acetest tablets in a urine sample.
Treatment
The general principle of direct energy supplementation is the same as outline for pregnancy toxaemia.
With non-pregnant animals, the second option is hormone therapy (cortisone) which affects the activity of certain key enzymes, thereby increasing the blood glucose supply.
In cases where problems with grain digestion are suspected, acidosis may be reduced by dosing the doe with sodium bicarbonate (500ml of a 5 per cent solution). A small dose of sodium bicarbonate (100 to 150ml) will stimulate the oesophageal groove to close, ensuring fluid flows directly to the fourth stomach. It is useful as a preliminary drench to be followed by the other forms of oral drenching outlined previously
http://www.acga.org.au/goatnotes/D010H.php
The clinical evidence of ketosis usually appears during the period leading up to peak lactation (six to eight weeks after kidding).
Sub-clinical form — Many high producing dairy animals are on the borderline for ketosis. Intermittent periods of indigestion may take place with excessive amounts of highly digestible food, which may result in high levels of volatile fatty acids. Excessive acidity is liable to cause a stand-still of rumen activity and a chain of metabolic events resulting in excessive fat breakdown and ketosis. In this mild form, does will have irregular milk production and days of inactivity.
Clinical form — In the more severe form, the clinical findings include:
- A decrease in appetite and milk production.
- A rapid loss in condition.
- Hard droppings which tend to have pointed ends.
- The doe is moderately depressed and frequently exhibits signs suggestive of milk abdominal pain.
- A "sweet corn" (acetone) smell may be detected on the doe's breath or in the milk.
Diagnosis is generally based on the doe's history (time of kidding) and the clinical findings. However, the clinical signs can be confused with hypocalcaemia (milk fever), enterotoxaemia (pulpy kidney), bloat, impaction, reticulitis and nephritis.
The presence of ketones can be established by using acetest tablets in a urine sample.
Treatment
The general principle of direct energy supplementation is the same as outline for pregnancy toxaemia.
With non-pregnant animals, the second option is hormone therapy (cortisone) which affects the activity of certain key enzymes, thereby increasing the blood glucose supply.
In cases where problems with grain digestion are suspected, acidosis may be reduced by dosing the doe with sodium bicarbonate (500ml of a 5 per cent solution). A small dose of sodium bicarbonate (100 to 150ml) will stimulate the oesophageal groove to close, ensuring fluid flows directly to the fourth stomach. It is useful as a preliminary drench to be followed by the other forms of oral drenching outlined previously
So sorry. Sometimes we do our best, it is just isn't happening. You did good. 
