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Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of volatile fatty acids by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.  
 
Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of volatile fatty acids by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.  
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Unlike in the glandular stomachs of carnivore and ominvores, the epithelium of the rumen is not protected by a layer of mucus. so they are vulnerable to chemical damage by acids. Low ruminal pH leads to rumenitis, erosion, and ulceration of the ruminal epithelium. Once the ruminal epithelium is inflamed, bacteria may colonize the papillae and leak into the portal circulation. These bacteria may cause liver abscesses, which may eventually lead to peritonitis around the site of the abscess. If the ruminal bacteria clear the liver (or if bacteria from liver infections are released into circulation), they may colonize the lungs, heart valves, kidneys, or joints. The resulting pneumonia, endocarditis, pyelonephritis, and arthritis are often difficult to diagnose antemortem. Postmortem evaluation of these conditions in animals that are slaughtered, culled, or that died on the farm can be very beneficial.
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Unlike in the glandular stomachs of carnivore and ominvores, the epithelium of the rumen is not protected by a layer of mucus. This means that ruminal epithelial cells are sensitive to chemical damage, for example in increased acidity. Low ruminal pH therefore leads to rumenitis, with erosion and ulceration of the ruminal epithelium. Bacteria can then colonise the ruminal papillae and be absorbedinto the portal circulation. This bacteraemia can seed infection to many tissues and can result in, for example, liver abscesses, pneumonia, endocarditis, pyelonephritis, or arthritis  if the liver, lunds, heart valves, kidneys or joints become infected. Any of these conditions are therefore potential complications of SARA.
Caudal vena cava syndrome can cause hemoptysis and peracute deaths due to massive pulmonary hemorrhage in affected cows. In these cases, septic emboli from liver abscesses can lead to lung infections, which ultimately invade pulmonary vessels and cause them to rupture.
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Subacute ruminal acidosis has also been associated with laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers. The severity of laminitis depends on the duration and frequency of metabolic insult. These foot problems generally do not appear until weeks or months after the initiating event. The mechanism by which subacute ruminal acidosis increases the risk of laminitis has not been fully characterized.
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Subacute ruminal acidosis has also been associated with coriosis (lamintis), hoof overgrowth and solar abscesses/ulcers, which may occure weeks to months following the inciting acidotic event. The mechanism of coriosis is currently poorly understood.
    
==Signalment==
 
==Signalment==
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