Lactic Acidosis is an acute metabolic disorder of ruminants, caused by ingestion of a large quantity of readily fermentable carbohydrate-rich feeds, and resultant production of lactic acid in the rumen. This condition is commonly observed in dairy cattle, feed-lots, and small ruminants which were recently shifted from green to concentrate feeds. Other common names for lactic acidosis are grain engorgement, grain overload, and rumen overload )

The amount and type of feed required to produce illness depends upon the type of the grain, previous adaptation, nutritional status and condition of the animal, and nature of the ruminal flora. Un-restricted or accidental access to excessive grains can lead to this condition. It can also occur after returning to grains folllowing a long off-feeding period.

NOTE: All kinds of grains are considered more toxic when finely ground or even crushed than whole grains as being readily exposed to micro-flora.

Pathogenesis

The normal ruminal environment is anaerobic, with a pH of 6.5, and comprises mainly bacterial and protozoal populations. Microbial digestion converts carbohydrates into volatile fatty acids (acetic acid, propionic acid, and butyric acid), carbon dioxide, and methane. After ingestion of excessive carbohydrate contents, there is a marked change in the species and number of the microbial population in the rumen. Gram-positive bacteria, such as Streptococcus Bovis, increases the number and convert the carbohydrates into large quantities of lactic acid and other organic acids.

Production of a large quantity of lactic acid decreases the pH of rumen below 5. At this pH, the growth of normal, and beneficial (lactate-utilizing bacteria) ruminal flora is destroyed. This pH also favors the lactobacilli to utilize the carbohydrates and produce an excessive quantity of lactic acid. Increased concentration of lactic acid and its salt causes osmotic pressure to rise and the movement of excessive fluid from systemic supplies into the rumen, causing fluid ruminal contents and dehydration. Low pH also causes rumenitis and absorption of the lactic acid and its salts, resulting in lactic acidosis and acidemia.

Clinical Signs

1. Diarrhea
2. Dehydration
3. Acidosis
4. Rumen enlargement & abdominal pain
5. Anorectic (off feed)
6. Once ill they do not drink water
7. Ruminal stasis
8. Heart rate increases
9. Shallow & rapid respirations
10. Temperature below normal (98°-101°F).
11. Feces have a sour-sweet odor & contain undigested kernels
12. Fluid Splashing sounds in the rumen on auscultation from the left flank
13. Severely affected animals have sluggish palpebral reflex 
14. Head turned into flank & animal resembles cases of parturient paresis.
15. Anuria is a common finding
16. Abortion also occurs after 10-14 days in pregnant animals

Treatment

Per acute cases should be considered for slaughtering otherwise vigorous therapy sholud be provided.

Withhold water and feed for such cases for next 24 hours, to avoid further engorgment or complications.

1. 5% solution of sodium bicarbonate should be administered through IV route at the rate of  5-10L/450kg. 
2. In the next 5-10 hours, administer electrolytes solutions or 1.3% sodium bicarbonate in saline.         (60L/450kg)
3. Procaine penicillin  G to avoid bacterial rumenitis. ( 5 days   IM.   22000U/Kg/day )
4. Thiamine.   IM ( Vitamin B1) to facilitate the lactate metabolism.