Diabetic lactic acidosis in the elderly

Introduction to lactic acid poisoning in the elderly Acidosis caused by elevated blood lactate levels for various reasons is called lactic acidosis. Health search lactic acidosis that occurs on the basis of diabetes is called diabetic lactic acidosis. Epidemiology: About 10% to 15% of people with ketoacidosis develop diabetes with lactic acidosis. Hyperosmolar non-ketotic diabetic coma patients have about 50% of both lactic acidosis. basic knowledge The proportion of illness: 0.005% Susceptible people: the elderly Mode of infection: non-infectious Complications: hypotension shock

The cause of diabetes lactic acidosis in the elderly

Poor diabetes control

Due to diet therapy, exercise therapy and drug treatment are not appropriate, diabetes control is poor, patients may have elevated blood sugar, dehydration and pyruvate oxidative disorders and lactic acid metabolism defects, leading to elevated blood lactate.

Take a large amount of phenformin

In particular, phenformin (hypoglycemic) can increase anaerobic glycolysis, inhibit liver and muscle lactic acid uptake, and inhibit gluconeogenesis, so it has the effect of causing lactic acidosis, improper selection in cases, such as advanced age, combined with cardiopulmonary liver Diabetic patients with kidney disease may have lactic acidosis if they use phenformin (hypoglycemic) in large doses.

Other diabetic acute complications

Such as infection, ketoacidosis and hyperosmolar non-ketotic diabetic coma and other acute diseases, can also be called the cause of diabetic lactic acidosis.

Other important organ diseases

Such as cerebrovascular accident, myocardial infarction, respiratory diseases, etc. can cause or aggravate poor blood perfusion of tissues and organs, leading to hypoxemia and lactic acidosis. Such as alcohol abuse, carbon monoxide poisoning, salicylic acid, catecholamines, lactose overdose can also induce lactic acidosis.

Pathogenesis

Lactic acid is the end product of glucose anaerobic glycolysis, which is reduced by pyruvate and has a molecular weight of 90. The lactic acid production sites in the body are mainly skeletal muscle, brain, red blood cells and skin. The main parts of lactic acid metabolism are liver and kidney. Under special circumstances, muscles can also be a place for lactic acid metabolism.

Under normal circumstances, the lactic acid produced during the metabolism of the body is mainly oxidized in the liver, or converted to glycogen for storage. A small amount of lactic acid is excreted from the urine by the kidney. The normal lactate concentration is 0.5-1.6 mmol/L (5~ 15mg/dl), no more than 1.8mmol/L, the normal kidney lactate threshold is 7.7mmol/L.

The anaerobic glycolysis of sugar is the oldest form of sugar metabolism that organisms have retained during long-term evolution. Even in highly evolved humans, it is still one of the important metabolic pathways. 1 mol of glucose can produce 2 mol of lactic acid and 2 mol of ATP by glycolysis. The main physiological significance is to ensure that the body can effectively obtain energy under anaerobic or hypoxic conditions, and it is also an important way for the body to generate energy to meet physiological needs under stress. Some tissue cells such as red blood cells, cornea, crystal, retina , testis, kidney medulla, etc., even rely on glycolysis to obtain energy even when aerobic, but when the supply of oxygen can not fully meet the metabolic needs, any tissue in the body can produce lactic acid.

First, 2 mol of pyruvate and 2 mol of ATP are produced by the common pathway of glycolysis and aerobic oxidation in the cytoplasm. When the oxygen supply is sufficient, the main pathway of pyruvate is transported by the specific pyruvate carrier on the mitochondrial inner membrane. Mitochondria, which is catalyzed by the pyruvate dehydrogenase complex on the mitochondrial membrane, further oxidizes to form acetyl-coenzyme, which is completely oxidized to CO2 via the tri-acid cycle and produces 36 mol of ATP, which can be split before pyruvate enters the mitochondria. It is lactic acid, and lactic acid is the end product of the glycolysis metabolic pathway. It can only be further metabolized after being converted into pyruvic acid by reverse reaction. Under physiological conditions, pyruvic acid and lactic acid are in a state of dynamic free equilibrium, and thus by NAD/NADH The ratio determines that the relative increase of NADH in the absence of O2 is beneficial to the formation of lactic acid. The pyruvate split is lactic acid, which prevents the oxidative metabolism in the mitochondria, so that 1 mol of glucose can only produce 2 mol of ATP, instead of aerobic metabolism. The 36 mol of ATP also produces 2 mol protons during the glycolysis process.

The increase in lactic acid production is not limited to the pathological state. Exercise can increase the formation of muscle lactic acid, which is the cause of muscle soreness caused by excessive exercise. When exercise is over, extra lactic acid is metabolized by conversion to pyruvate, which is consumed in the process. Additional protons and the production of bicarbonate, so that possible acidosis can be corrected spontaneously, alcohol abuse may increase the production of lactic acid, but alcoholism itself is not enough to cause severe lactic acidosis, unless accompanied by poorly controlled diabetes, In the case of significant hypovolemia or advanced liver disease, lactic acidosis can be quite severe.

In healthy adults, the rate of lactic acid production is 0.8mmol (kg) on average, or 1150mmol/d in 60kg normal people. The lactic acid produced by the body must be metabolized at the same rate to not accumulate in the body. Many tissues can participate in lactic acid metabolism. Among them, liver and kidney have the strongest metabolic capacity, and the lactic acid metabolism declines when liver and kidney are insufficiency, which can cause lactic acid to accumulate in the body, leading to lactic acidosis. Many factors causing excessive lactic acid production are insufficient to form lactic acid when liver and kidney function is normal. Poisoning, and in the case of liver and kidney dysfunction, lactic acidosis is very easy to occur, so even in patients with mild liver and kidney dysfunction, biguanide drugs are contraindicated.

In severe lactic acidosis, myocardial contractility and arteriolar tension are weakened, often accompanied by hypotension or even shock, which in turn causes tissue perfusion deficiency, aggravates lactic acidosis, and forms a vicious circle, a multicenter clinical study (total 255 For example, the survival rate of lactic acidosis is not only related to blood lactic acid concentration and pH value, but also significantly related to arterial systolic blood pressure. Before treatment, the systolic blood pressure <12.0 kPa (90 mmHg), the survival rate at 72 h is only 12.5%; For patients with a pressure >12.0 kPa (90 mmHg), the survival rate at 72 h was 55%. Multiple organ failure was another serious consequence and cause of death in lactic acidosis. In this group of patients, about half of the patients occurred at the beginning of admission (or more than 4). The system of multiple organ failure, multiple organ failure before death, almost inevitable outcome.

The mortality rate of lactic acidosis caused by different causes is not the same. The prognosis of shock is the worst, while the cause of biguanide is relatively good. The mortality rate of lactic acidosis caused by metformin is 50%.

Elderly people with diabetes lactic acid poisoning prevention

With the development of economic development and urbanization, diabetes and complications have become a major problem that has seriously jeopardized people's health. The rate of diabetes patients has more than tripled in China in the past 20 years. It is predicted that by 2020, the total population of China will increase to 2020. 1.5 billion, 60-year-olds will reach more than 200 million, and the impact of diabetes on the health of the Chinese people will become more and more serious. Although diabetes is not the main cause of death in China, it seriously endangers human health and life complications. It has a significant impact on the lives of Chinese people and has multiplied, especially in cities, in the elderly group. However, due to the complexity of the etiology and pathogenesis of diabetes, we cannot hope that the treatment of diabetes will occur in a short period of time. Fundamental changes, therefore, we need to understand the impact of diabetes and its complications on Chinese health, and take appropriate preventive measures to reduce the incidence of diabetes and its complications, to ensure that most people enjoy a healthy life and work, Therefore, according to the current status of diabetes prevention and control in China, the following basic tasks should be vigorously strengthened.

1. Conducting publicity and education on diabetes

First, improve the awareness of diabetes prevention and treatment among all clinical medical staff including diabetes professionals, improve the treatment of diabetes, prevent the occurrence and development of complications, and secondly, strengthen the education of diabetes and their relatives and friends on diabetes knowledge and improve diabetes. The patient's ability to self-monitor and treat, once again, raises the awareness and attention of diabetes in the whole society, strengthens the education of diabetes, helps, and strengthens the society's attention and support for diabetes.

2. Extensively carry out three-level prevention and treatment of diabetes by means of community prevention and treatment

Primary prevention: It is a non-selective prevention for the entire population, with the aim of reducing the incidence of diabetes. The main measures are to change environmental factors and lifestyles, such as appropriate energy intake, avoid obesity and encourage more Physical activity, etc., the implementation of this measure generally requires the government and the health department to attach great importance to it, as a national policy, using the media to extensively and thoroughly carry out social education, the first-level prevention of type 1 diabetes, some scholars recommend the companion Islet cell antibodies and/or glutamate decarboxylase antibody-positive first-degree relatives of type 1 diabetes are treated with immunological intervention to prevent or delay type 1 diabetes.

Secondary prevention and treatment: high-risk groups of type 2 diabetes (mainly including family history of type 2 diabetes, hypertension, hyperlipidemia, obesity or overweight and gestational diabetes women over 40 years old), as well as early detection of asymptomatic Interventional therapy and management of type 2 diabetes and IGT to prevent or reduce the occurrence of diabetic complications, prevent or delay the transition of IGT to type 2 diabetes, IGT is intermediate between normal and type II diabetes, and the rate of IGT patients The level of diabetes is parallel to the prevalence of diabetes, but it is not completely consistent. It is generally believed that about one-third of IGT patients change to diabetes every 5 to 10 years, 1/3 turn to normal, and 1/3 are still IGT. The factors affecting the outcome of IGT are more complicated. Multivariate analysis found that only OGTT 1h blood glucose, 2h blood glucose, BMI, UAE and Hb A1c are independent risk factors for predicting the conversion of IGT patients to diabetes. And the two aspects of drug intervention, the former includes limiting the total calorie intake, reducing the fat in the diet, especially the content of saturated fatty acids, increasing the proportion of complex carbonated water compounds and the content of dietary fiber and Add physical activity, etc.; the latter recommended the use of metformin, acarbose and insulin sensitizers, etc. The secondary prevention of type 1 diabetes is mainly to identify the early stage of clinical symptoms from type 2 diabetes as early as type 2 Patients with type 1 diabetes with slow progression of diabetes have early protection from insulin and have a protective effect on their residual B cell function, which can prevent or delay their progression to complete type 1 diabetes.

Three levels of prevention and treatment: for patients with diagnosed diabetes, comprehensive treatment to prevent or delay their complications, mainly chronic complications, can generally take active control or eliminate the risk factors associated with complications; Early treatment; pay attention to the monitoring of people susceptible to acute complications of diabetes to reduce the death of diabetic patients.

3. In-depth study of the pathogenesis of diabetic complications

Especially in the case of the general screening and prevention of diabetes in China, the clinically seen diabetic patients often come to see a doctor because of various complications. Therefore, while improving the treatment of diabetes by clinicians, the incidence of diabetes complications should be strengthened. Mechanism research to find more effective prevention and treatment strategies.

In the diagnosis and treatment of elderly patients, regardless of whether the patient has a history of diabetes, care should be taken to avoid factors that may lead to the disease and prevent the occurrence of this disease.

(1) Early detection and strict control of diabetes, the incidence of diabetes in the elderly is on the rise, and increases with age, more than 50% of people over 50 years old, the elderly should regularly check blood sugar for early detection and early treatment asymptomatic Sexual diabetes is especially important.

(2) Prevention and treatment of various infections, stress, high fever, gastrointestinal water loss, etc., which may lead to hyperglycemia and severe dehydration, so as to avoid hyperosmolar state or ketoacidosis.

(3) Pay attention to all kinds of drugs that cause diarrhea in elderly patients, such as diuretics and blood glucose drugs, biguanides and glibenclamide, pay attention to the blood pressure when dehydration therapy is applied, pay attention to water loss during dialysis, and try to prevent the induction of senile diabetes coma. .

Elderly diabetic lactic acid poisoning complications Complications, hypotension, shock

Mainly complicated by hypotension and shock, multiple organ failure and so on. Shock is a clinical syndrome characterized by acute and effective circulating blood volume caused by various serious pathogenic factors, with neuro-humoral factor imbalance and acute circulatory disorder. These pathogenic factors include major bleeding, trauma, poisoning, burns, asphyxia, infection, allergies, and heart pump failure. Multiple organ failure (MOF) is a clinical syndrome with a wide range of causes, complicated pathogenesis, and high mortality.

Symptoms of Diabetes in the elderly, lactic acidosis, common symptoms, diabetes, fatigue, lethargy, sleepiness, nausea, anorexia, coma, shock, kidney failure

Symptoms and signs: The incidence of lactic acidosis is more urgent, but the symptoms and signs may not be specific. Clinical manifestations of lactic acidosis are often masked by primary or induced diseases, which may cause misdiagnosis or missed diagnosis. The clinical manifestations of mild cases are not obvious. Only breathing slightly deeper; moderate and severe can be fatigue, weakness, nausea, anorexia or even vomiting, deep breathing without ketone odor, blood pressure and body temperature can be reduced, often sleepy, lethargy, consciousness blindness, lethargy, Severe cases can be deep coma or shock.

New point of view: The key to diagnosing lactic acidosis is to have sufficient vigilance against this disease. In shock state with acidosis, it can be diagnosed as lactic acidosis without blood lactic acid determination; The diagnosis of poisoned patients needs to be based on blood lactic acid determination.

Examination of diabetes lactic acidosis in the elderly

Urine sugar and urinary ketone (-) ~ (+), normal blood osmotic pressure, blood CO2cp decreased (up to 10mmol / L or less), pH value decreased significantly, anion gap expanded (up to 20 ~ 40mmol / L or less), blood lactate Significantly increased levels are the key diagnostic basis for this disease. Patients with blood lactic acid above the upper limit of normal, more than 5mmol / L, it is worth noting that lactic acidosis is sometimes accompanied by ketoacidosis and hyperosmolar nonketotic diabetic coma Existence, thus increasing the complexity of the diagnosis, in addition to acidosis caused by other causes such as uremia and salicylic acidosis.

Chest X-ray examination, normal heart and lung.

Diagnosis and diagnosis of lactic acidosis in elderly patients with diabetes

Diagnostic criteria

New points in the diagnosis of lactic acidosis in diabetes include:

1. Have a history of diabetes

However, most patients have low blood sugar levels and no significant ketoacidosis.

2. Evidence of acidosis

Such as pH <7.35, blood bicarbonate <20mmol / L, anion gap > 18mmol / L, etc., if the diagnosis of ketoacidosis, renal failure can be ruled out, the possibility of lactic acidosis should be highly considered.

3. Increased blood lactate levels

Above 1.8mmol / L, blood lactate levels of 2 ~ 5mmol / L, patients are more compensatory acidosis, this only lactic acid is too high and no acidosis can be called hyperlactosis, lactic acid The blood lactate level of poisoned patients exceeds 5mmol/L, which is the main basis for the diagnosis of lactic acidosis.

Differential diagnosis

Clinically, it must be differentiated from diabetic ketoacidosis and diabetic hyperosmolar coma.

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