Lactic acidosis and hyperlactacidemic coma

Lactic acidosis is a state of metabolic acidosis that results from an increased content of lactic acid in the blood. Lactic acidosis is not a specific complication of diabetes. This state is of a polytechological nature. The development of lactic acidosis can be triggered by various diseases and conditions that are accompanied by tissue hypoxia, as well as an increase in the intensity of formation and a decrease in the utilization of lactate. In cases involving tissue hypoxia, type-A lactation doses develop. This can be with cardiogenic, endotoxic, hypovolemic shock, anemia, carbon monoxide poisoning, epilepsy or pheochromocytoma. In pathological conditions characterized by increased formation and decreased utilization of lactate, lactic acidosis of type B1 develops. This is characteristic of renal or hepatic failure, oncological diseases and hemoblastosis, severe infections, and decompensated diabetes mellitus. Type B2 lactic acidosis develops when using biguanides, poisoning with methanol or ethylene glycol, cyanides, with excessive parenteral administration of fructose. It is also possible to develop lactic acidosis of type B3, which occurs in hereditary metabolic disorders, for example, when there is a deficit of glucose-6-phosphate-dehydrogenase or methylmalonic acidemia.

Lactate is a metabolic product that is directly involved in the metabolism of carbohydrates. Lactate, along with pyruvate, is a substrate for glucose synthesis in the process of neoglucogenesis. The formation of lactate increases with the development of hypoxia, when aerobic is inhibited and anaerobic glycolysis is activated. The end product of anaerobic glycolysis is lactic acid. At the same time, lactate is synthesized in the body faster than turns into pyruvate, and is utilized in the process of neoglyukogens. Normally, the ratio of lactate and pyruvate is expressed as 10: 1. More frequent development of lactic acidosis in diabetes mellitus is explained by the fact that its frequent decompensation contributes to the state of chronic hypoxia as a result of an increase in the level of glycated hemoglobin, which has a positive effect.
higher affinity for oxygen.

In addition, quite often patients with diabetes mellitus II

Pas, especially the elderly, have several associated diseases. Most often such diseases are pathologies of the cardiovascular system, which are characterized by a state of chronic hypoxia. The state of severe hypoxia usually accompanies such acute complications of diabetes mellitus as ketoacidotic and hyperosmolar coma. In these cases, the resulting lactic acidosis aggravates the already serious condition of the patients. In addition, their life expectancy becomes more unfavorable. As a result of insulin deficiency in diabetes mellitus, the level of muscular pyruvate dehydrogenase decreases, which leads to an increase in lactate synthesis and the creation of prerequisites for the development of type B lactic acidosis.

The most common cause of lactic acidosis in diabetes mellitus is the intake of glucose-lowering drugs from the bi-guanide group, such as phenformin and buformin. These drugs have the ability to activate anaerobic glycolysis in the small intestine and muscles, which, in turn, leads to an increase in lactate production and inhibition of gluconeogenesis in the liver. Currently, these drugs are not available. The current drug of the biguanide group is metformin. This drug does not cause such a pronounced accumulation of lactate due to other structural and pharmacokinetic features. By their nature, lactic acidosis in most cases has a mixed origin, that is, it is type A + type B. Several factors take part in the pathogenesis of mixed lactic acidosis. In this case, a more significant role is played by comorbidity, which is accompanied by hypoxia, as well as decompensation of diabetes mellitus. Against the background of these changes, anaerobic glycolysis is activated in the body, which is accompanied by the formation of an excess of lactate. An important addition
The main factor in the pathogenesis of lactic acidosis is the addition of renal pathology, which leads to a worsening of lactate excretion from the body.


Lactic acidosis is initially manifested by increased fatigue, increasing weakness, drowsiness, nausea, and vomiting. These symptoms resemble decompensation of diabetes mellitus. The main symptom that can be caused by the eyesight in relation to lactic acidosis is the appearance of muscle pain, which is caused by the accumulation of lactic acid in them. Severe metabolic acidosis in patients with diabetes mellitus can develop in just a few hours. Usually, its symptoms are Cussmaul breathing, dilated peripheral vessels, a sharp decrease in blood pressure, cardiac rhythm disturbances, confusion, stupor or

local_offerevent_note May 30, 2019

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