Symptoms in humans include all those of typical metabolic acidosis (nausea, vomiting, generalized muscle weakness, and laboured and deep breathing). Causes
The several different causes of lactic acidosis include:
Genetic conditions
Biotinidase deficiency, multiple carboxylase deficiency, or nongenetic deficiencies of biotin
Diabetes mellitus and deafness
Fructose 1,6-bisphosphatase deficiency
Glucose-6-phosphatase deficiency
GRACILE syndrome
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes
Pyruvate dehydrogenase deficiency
Pyruvate carboxylase deficiency
Leigh syndrome
Drugs
Linezolid
Paracetamol/acetaminophen poisoning
Metformin: this risk is low (less than 10 cases for 100,000 patient years), but the risk of metformin-induced lactic acidosis (MALA) increases in certain situations where both the plasma levels of metformin are increased and lactate clearance is impaired. The older related and now withdrawn drug phenformin carried a much higher risk of lactic acidosis. Isoniazid toxicity
Propofol
Epinephrine
Propylene glycol (D-lactic acidosis)
Nucleoside reverse-transcriptase inhibitors
Abacavir/dolutegravir/lamivudine
Emtricitabine/tenofovir
Potassium cyanide (cyanide poisoning)
Fialuridine
Other
Thiamine deficiency (especially during TPN)
Impaired delivery of oxygen to cells in the tissues (e.g., from impaired blood flow (hypoperfusion))
Bleeding
Polymyositis
Ethanol toxicity
Sepsis
Shock
Advanced liver disease
Diabetic ketoacidosis
Excessive exercise (overtraining)
Regional hypoperfusion (e.g., bowel ischemia or marked cellulitis)
Cancers such as Non-Hodgkins and Burkitt lymphomas
Pheochromocytoma
Tumor lysis syndrome
D-lactic acidosis due to intestinal bacterial flora production in short gut syndrome

Pathophysiology
Glucose metabolism begins with glycolysis, in which the molecule is broken down into pyruvate in ten enzymatic steps. A significant proportion of pyruvate is converted into lactate (usually 10:1). The human metabolism produces about 20 mmol/kg of lactic acid every 24 hours. This happens predominantly in tissues (especially muscle) that have high levels of the "A" isoform of the enzyme lactate dehydrogenase (LDHA), which predominantly converts pyruvate into lactate.
Both L and D isomers of lactic acid are produced in the rumen; these isomers are metabolized by different metabolic pathways, and activity of the principal enzyme involved in metabolism of the D isomer declines greatly with lower pH, tending to result in an increased ratio of D:L isomers as acidosis progresses.Measures for preventing lactic acidosis in ruminants include avoidance of excessive amounts of grain in the diet, and gradual introduction of grain over a period of several days, to develop a rumen population capable of safely dealing with a relatively high grain intake. Administration of lasalocid or monensin in feed can reduce risk of lactic acidosis in ruminants,  inhibiting most of the lactate-producing bacterial species without inhibiting the major lactate fermenters. Also, using a higher feeding frequency to provide the daily grain ration can allow higher grain intake without reducing the pH of the rumen fluid.Treatment of lactic acidosis in ruminants may involve intravenous administration of dilute sodium bicarbonate, oral administration of magnesium hydroxide, and/or repeated removal of rumen fluids and replacement with water (followed by reinoculation with rumen organisms, if necessary). References


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