Lactic acidosis


Introduction to lactic acidosis

Lactic acidosis (LA) is a rare and serious acute complication of diabetes. Once it occurs, the mortality rate can be as high as 50% or more, especially blood lactate >25mmol/L, and the mortality rate is as high as 80%. The plasma lactic acid concentration depends on the rate of glycolysis and lactic acid utilization, and the blood lactic acid concentration is increased due to various reasons such as hypoxia, excessive production of lactic acid, or reduction of lactic acid utilization and clearance due to diseases such as liver and kidney.

basic knowledge

The proportion of illness: 15%

Susceptible people: no special people.

Mode of infection: non-infectious

Complications: coma


Cause of lactic acidosis

According to the pathogenesis, it can be divided into two categories:

1, type A due to lack of O2, seen in a variety of shock (cardiac, endotoxin, hypovolemia), anemia, heart failure, asphyxia, CO poisoning.

2, B type is divided into three types:

Type B1 is caused by systemic diseases, found in diabetes, malignant tumors (leukemia, etc.), liver disease (acute viral or toxic hepatitis with functional failure), severe infection (sepsis, etc.), uremia, convulsions, pancreatitis and stomach Enteropathy and so on.

Type B2 is caused by drugs and toxins, especially in biguanides, fructose, sorbitol, xylitol, methanol, ethanol, acetol (paracetamol), salicylate and ethylene glycol.

Type B3 is caused by glucose 6-phosphatase deficiency (type 1 glycogen accumulation disease), pyruvate dehydrogenase and carboxylase deficiency, fructose 1,6 diphosphatase deficiency, and oxidative phosphorylation defects due to abnormal metabolism.


Lactic acidosis prevention

It is very important to prevent this disease. The following points should be noted:

1. Control diabetes Diabetes patients with poor diabetes can be treated with insulin. Other complications of diabetes such as infection, ketoacidosis, diabetes non-ketotic hyperosmolar syndrome can also induce lactic acidosis, so it should actively treat diabetes and prevent secondary infection.

2. Anyone with liver and kidney dysfunction who is refrained from using bismuth-like diabetes with pyelonephritis and glomerulosclerosis may cause sputum accumulation; patients with recessive coronary heart disease may also have heart failure or renal dysfunction. Affects its excretion with hypoxia. Therefore, it is necessary to identify the heart, liver and kidney function before using drugs such as biguanides. The chance of developing this disease is significantly lower than that of phenformin (hypoglycide).

3. Actively treat various diseases that can induce lactic acidosis, such as myocardial infarction and carbon monoxide poisoning. If there is acidosis in the case of shock, lack of O2, liver and kidney failure, it is necessary to be alert to the possibility of this disease.

4. Diabetes patients should abstain from alcohol, and try not to use alcohol drugs such as sorbitol, xylitol, methanol, and ethanol.


Complications of lactic acidosis Complications

Poisoning coma, high mortality.


Symptoms of lactic acidosis Common symptoms Nausea abdominal pain Cardiotoxicity Drowsiness coma Defiance Imagination Acne

Depending on the cause of the disease, hypoxia caused by cyanosis, shock and other primary manifestations, drug-induced people often take medication or alcohol and other medical history and various poisoning performance, caused by systemic diseases, in addition to the primary disease In addition to symptoms, acidosis is the main cause, the onset is more urgent, there are deep breathing, confusion, drowsiness, stupor, coma and other symptoms, sometimes accompanied by nausea, vomiting, abdominal pain, but no purpura, signs of shock.


Examination of lactic acidosis

Urine and blood acidity increased significantly, blood pH <7.0, CO2 binding capacity decreased to less than 20% by volume, blood lactate >5mmol / L, sometimes up to 35mmol / L (>25mmol / L are mostly cured), pyruvic acid also increased Up to 0.2 ~ 1.5mmol / L, lactic acid / pyruvic acid 30/1, HCO-3 decreased, Na +, Cl - little change, Na + sometimes high, K + often increased or normal, anion gap [Na + + K + - ( HCO-3 dec-) is often >18mmol/L, generally 25-45, but the ketone body is not much increased, according to which lactic acidosis can be diagnosed.

In this disease, the white blood cells are mostly increased, sometimes up to 60,000/mm3. For example, patients with oral biguanide have severe acidosis and the ketone body is not significantly increased. This disease should be suspected and the lactic acid should be measured. Confirmed diagnosis.


Diagnosis and identification of lactic acidosis

Differential diagnosis

Hyperosmolar non-ketotic diabetic coma patients may also have dehydration, shock, coma and other manifestations, more common in the elderly, but blood glucose often exceeds 33.3mmol / L, blood sodium exceeds 155mmol / L, plasma osmotic pressure exceeds 330mmol / L The blood ketone body is negative or weakly positive.

Lactic acidosis, such patients have acute onset, infection, shock, history of hypoxia, acidosis, rapid breathing and dehydration. Although blood glucose is normal or elevated, blood lactate is significantly elevated (more than 5mmol). /L), the anion gap exceeds 18 mmol/L.

Alcoholic acidosis has the habit of drinking alcohol, and it is often caused by heavy drinking. The patient's blood -hydroxybutyrate is elevated due to hyperemesemia, and blood ketone may be positive, but the osmotic pressure is increased while acidosis and anion gap increase. Also rising.

Hunger ketosis is caused by insufficient eating. The patient's fat is decomposed and blood ketone is positive, but urine sugar is negative and blood sugar is not high.

Patients with hypoglycemia and coma have had too little food intake, acute onset, drowsiness, coma, but urine sugar, urine ketone negative, low blood sugar, excessive overdose of insulin or excessive intake of hypoglycemic drugs.

Acute pancreatitis more than half of patients with diabetic ketoacidosis will have blood, urine amylase non-specific increase, and sometimes its increase is large, the author has diagnosed a patient with diabetic ketoacidosis, blood, urine amylase All up to 3000U, but no abdominal pain, abdominal soft and no tenderness, abdominal CT scan of the pancreas without edema, exudation and other inflammatory manifestations, not fasted, after 3 to 4 days, blood, urine amylase decreased to normal, so can not be based solely on amylase If you are elevated, you will be diagnosed with acute pancreatitis. However, it should be noted that some patients may have acute pancreatitis at the same time, and even start with acute pancreatitis. Therefore, changes in amylase should be considered in combination with clinical considerations, and there is abdominal pain in the onset. Abdominal CT scans were performed in patients with elevated amylase, and close follow-up. About 50% of patients with acute pancreatitis developed temporary mild hyperglycemia, but with the recovery of pancreatitis, most patients had decreased hyperglycemia within 2-6 weeks. However, patients with acute hemorrhagic necrotic pancreatitis have large pieces of hemorrhagic necrosis of pancreatic tissue, and there are damage to islet B cells, the degree of damage and the severity and duration of glucose metabolism disorders in patients. For such serious damage islet B cells, can be complicated by diabetic ketoacidosis.