Lactic acid is a product of carbohydrate hypoxia metabolism, and lactic acid production increases when tissues are hypoxic. When suffering from excessive lactic acid accumulation, which conditions should be differentially diagnosed: 1. Clinically, patients who are comatose, dehydrated with acidosis and in shock, especially those with unknown causes, ketone smell in breath, low blood pressure and still high urine volume, should be alerted to the possibility of the presence of lactic acidosis. Some patients with diabetes mellitus combined with DKA alone; some with diabetes mellitus combined with other diseases such as uremia, cerebrovascular accident and other coma; some or coma due to other diseases and then induced ketoacidosis, should be carefully distinguished. Generally, through medical history, physical examination and laboratory tests of urine glucose, urine ketone glucose, blood ketone and carbon dioxide binding force blood gas analysis, most of them can be clearly diagnosed. 2. Differentiate from DKAHNDC and LA caused by acute metabolic disorders of diabetes mellitus and acute complications of diabetes mellitus hypoglycemic coma. LA due to acute metabolic disorder of diabetes: It is a metabolic complication of diabetes caused by the blockage of glucose oxygenation process, increase of glucose glycolysis and production of large amount of lactic acid, which makes the synthesis of lactic acid greater than the degradation and excretion of lactic acid gathering in the body. Lactate is the end product of anaerobic glucose enzymes and is produced by the reduction of pyruvate. The breakdown of glucose is divided into aerobic oxidation and anaerobic enzymes. Aerobic oxidation means that it is the main pathway for energy production from the breakdown of sugar in the body. Under anaerobic conditions, glucose is enzymed in the cytosol and its intermediate product pyruvate is converted to lactate by hydrogenation of reduced coenzyme I (NADH) and NADH to coenzyme I (NAD+) by the action of lactate dehydrogenase. Lactate can also be oxidized to pyruvate when NAD+ is converted to NADH by the action of lactate dehydrogenase, which is a reversible reaction catalyzed by lactate dehydrogenase. Under aerobic conditions, pyruvate can enter the mitochondria for further oxidation, which is catalyzed by pyruvate carboxylase to produce acetyl coenzyme A, which is then decomposed to H2O and CO2 by the oxidative capacity of the tricarboxylic acid cycle. pyruvate can also be isomerized to glucose by the pyruvate carboxylation branch. The main sites of lactate production in the body are skeletal muscle, brain, red blood cells and skin; the main sites of metabolic clearance are the liver and kidney. Under normal conditions, lactic acid produced during metabolism is mainly oxidized and utilized in the liver or converted to glycogen for storage, while a small amount of lactic acid is excreted via the kidneys. Therefore, insufficient lactate clearance is more commonly associated with liver disease, with cirrhosis of the liver being the most common. Glycosuria hypoglycemia: The symptoms manifest differently, with most feeling weak and difficult to support. Sympathetic excitatory symptoms and central nervous system manifestations are usually present. Hormones play an important role in the regulation of blood glucose concentration as well as glucose metabolism. Insulin is the only glucose-lowering hormone in the body, and it is also the hormone that plays a dominant role in the regulation of the body within the normal blood glucose range. There are many types of glucose-raising hormones, with different mechanisms of action and glucose-raising effects. The main ones are hyperglycemia, epinephrine, noradrenaline and glucocorticoids. During hypoglycemia, the release of these hormones increases, and the blood glucose concentration rises rapidly, exerting a counter-regulatory effect on hypoglycemia. In addition, ACTH and β-endorphin play a counter-regulatory role mainly by promoting the release of cortisol. The glucose-raising effect of physiological doses of prolactin is not significant. The onset of hypoglycemia in glycosuria is very insidious and sometimes difficult to detect at the beginning. Patients with brittle glycosuria are prone to sudden attacks, most of which occur acutely. The clinical manifestations of senile hypoglycemia are often not typical enough and should be detected only by careful examination.