Bovine lactic acidosis syndrome is associated with large increases of
lactic acid in the rumen, which result from diets that are high in rum
inally available carbohydrates, or forage that is low in effective fib
er, or both. The syndrome involves two separate anatomical areas, the
gastrointestinal tract and body fluids, and is related to the rate and
extent of lactic acid production, utilization, and absorption. Clinic
al manifestations range from loss of appetite to death. Lactic acid ac
cumulates in the rumen when the bacteria that synthesize lactic acid o
utnumber those that utilize lactic acid. The systemic impact of acidos
is may have several physiological implications, including laminitis, a
diffuse aseptic inflammation of the laminae (cerium). Although a nutr
itional basis for the disease exists, etiology includes a multitude of
interactive factors, such as metabolic and digestive disorders, postp
artum stress, and localized trauma, which lead to the release of vasoa
ctive substances that trigger mechanisms that cause degenerative chang
es in the foot. The severity of laminitis is related to the frequency,
intensity, and duration of systemic acidotic insults on the mechanism
s responsible for the release of vasoactive substance. The critical li
nk between acidosis and laminitis appears to be associated with a pers
istent hypoperfusion, which results in ischemia in the digit. Manageme
nt of acidosis is critical in preventing laminitis. High producing dai
ry herds attempting to maximize energy intake are continually confront
ed with subclinical acidosis and laminitis. Management of feeding and
husbandry practices can be implemented to reduce incidence of disease.