Diabetes mellitus leads to

Type A Lactic acidosis Shock, Anemia, Mitochondrial Damage - Cyanide poisoning Type B Lactic acidosis DM, CRF, Malignancy,Metformin, Seizures Type D Lactic acidosis D- Lactate product by bacteria, Sho bowel syndrome, Intestinal Obstruction, Jejunoileal bypass Lactic acid is the end product of the anaerobic metabolism of glucose. Normally, the principal sources of this acid are the erythrocytes (which lack the enzymes for aerobic oxidation), skeletal muscle, skin, and brain. The chief pathway for removal of lactic acid is by hepatic (and to some degree renal) uptake for conversion first to pyruvate and eventually back to glucose, a process that requires oxygen. Lactic acidosis occurs when excess lactic acid accumulates in the blood. This can be the result of overproduction (tissue hypoxia), deficient removal (hepatic failure), or both (circulatory collapse). Lactic acidosis is not uncommon in any severely ill patient suffering from cardiac decompensation, respiratory or hepatic failure, septicemia, or infarction of the bowel or extremities. Type A lactic acidosis is associated with tissue hypoxia from hypovolemia or endotoxic shock and need not be associated with hyperglycemia. Type B lactic acidosis is defined as that which occurs in the absence of clinical evidence for tissue hypoxia and is associated with diabetes per se or with biguanide therapy. With the discontinuance of phenformin therapy in the United States, lactic acidosis in patients with diabetes mellitus has become uncommon, but it still must be considered in the acidotic diabetic patient if the patient is seriously ill, and especially if the patient is receiving metformin therapy as well. Most cases of metformin-associated lactic acidosis occur in patients in whom there were contraindications to the use of metformin, in paicular renal failure.