Mertabolic disease List of metabolic diseases

What is Metabolic Disease? About Metabolic Diseases

Metabolic Disease Meaning: The body’s metabolism includes two processes, anabolic and catabolic. The former is the synthesis of macromolecular substances from simple ingredients to maintain tissue structure and function. The latter is the decomposition of large molecular substances into small molecular substances, which mainly provide the energy required by the body. The main metabolites are carbohydrates, fats, and proteins. The metabolic processes of these three cannot be separated. Metabolic diseases are disturbances in the process of material metabolism, mostly caused by abnormal enzymes or proteins.

There are about one hundred kinds of human enzymes that are changed, which almost affect the functions of tissues and organs in the body. The clinical can be divided into the following two categories:

  i. Congenital deficiency, some hereditary chromosomal abnormalities, a wide range, but the incidence is not high, such as glycogen storage disease, familial hypercholesterolemia, familial hyperglycerol Lipidemia, gout, etc. The clues suggested by clinical manifestations and the determination of specific metabolites are not difficult to diagnose, but are rare and prone to delay diagnosis.

ii. Symptoms are metabolic disorders, and many other systemic diseases may cause the body’s metabolic abnormalities at a certain stage, which complicates the clinical manifestations and diagnosis and treatment. Electrolyte disorders and hypoproteinemia may occur in the advanced stage of renal disease; hypothyroidism is often accompanied by hyperlipidemia, and excessive adrenal glucocorticosterone can cause negative nitrogen balance.


Section 2 Diabetes (Diabetas Mullitus, a metabolic disease)

Diabetes is a group of endocrine-metabolic diseases characterized by hyperglycemia. It is characterized by the absolute or relative lack of insulin and the reduced sensitivity of target cells to insulin, causing metabolic disorders of carbohydrates, proteins, fats, electrolytes and water.

The incidence of diabetes is high. The incidence of the general population in USA is 8-12%, while West Virginia has above 16% and the incidence of it in the elderly is higher.

Even in China, since the liberation, with the improvement of people’s living standards, it has gradually increased. Before the liberation of urban residents, it was less than 1% (Beijing), now it is 1-2%, those over 40 years old is 3-4%, and individual reported retirement cadres can reach 12%. Rural and mountainous areas are lower than cities. The incidence rate in western industrial countries is 2-4%. Early diabetes has no obvious clinical symptoms and is not easy to detect. A large number of people with diabetes in China and western industrial countries have not been able to obtain timely diagnosis and treatment.

Due to the many complications of diabetes and the lack of effective preventive measures at present, if it is allowed to develop, it will become an irreversible change that can lead to sickness or death of patients. Therefore, to raise awareness of diabetes, attach importance to early diagnosis, effectively prevent and prevent Treatment and morbidity are issues worthy of attention today.


Types of diabetes (Metabolic Disease)

According to the 1980 World Health Organization Geneva meeting, the diabetes classification made.

 In order to make it easier to consult the literature and avoid confusion about the categorized nouns of diabetes, a list of nouns that are basically similar in the past is as follows:


Classification of Diabetes and Other Impaired Glucose Tolerance

I. Clinical types

(A) diabetes


Insulin-dependent diabetes mellitus


Non-insulin-dependent diabetes mellitus






Malnutrition-related diabetes


Other types, including diabetes with other conditions and syndromes

(1) pancreatic disease

(2) endocrine disease

(3) drug-derived or chemically-induced

(4) insulin or other receptor abnormalities

(5) certain genetic syndromes

(6) other


(B) Abnormal glucose tolerance in this metabolic disease


Non-obese in this metabolic disease


Obesity in this metabolic disease


With other conditions or syndromes, as with other types mentioned above

(C) Gestational Diabetes *


2. Statistical risk types (normal glucose tolerance)

(A) have had impaired glucose tolerance **

(B) Potential potential for abnormal glucose tolerance ***


* Gestational diabetes refers to diabetes that occurs or is discovered during pregnancy. Female patients with diabetes do not include subsequent pregnancy. The outcomes of gestational diabetic patients after childbirth are different and must be re-examined. Most patients (approximately 70%) return to normal glucose tolerance after delivery, and can be classified as “experienced with impaired glucose tolerance”. A small number of patients still have diabetes or impaired glucose tolerance after delivery.


** The patient had impaired glucose tolerance or gestational diabetes or diabetes in the past, and recovered naturally or after treatment. The glucose tolerance is normal.


*** Previously named Diabetes Tendency, No Impaired Glucose Tolerance or History of Diabetes (metabolic disease).


Comparison of Names of Types of Diabetes

Classification name in use

Insulin-dependent diabetes mellitus

Non-insulin-dependent diabetes Adult-onset diabetes, Adolescent adult-onset diabetes (MODY)


Other types of secondary diabetes (metabolic disease)

Impaired glucose tolerance asymptomatic diabetes, chemical diabetes, subclinical diabetes *

Gestational diabetes : Gestational diabetes (metabolic disease)

Previously abnormal glucose tolerance, hidden diabetes, pre-diabetes

Potential for impaired glucose tolerance

* Some of them are non-insulin-dependent diabetes.


The above classification only indicates the clinical type, which does not indicate the difference in etiology and pathogenesis, and the non-insulin-dependent type may change to insulin-dependent type. Some patients are difficult to distinguish.


Differentiation between insulin-dependent and non-insulin-dependent diabetes


Insulin-dependent diabetes mellitus

a. The main conditions in this metabolic disease

Significant decrease in plasma insulin Mild decrease, normal or high

Insulin release test Low response or no response Delayed response

Anti-insulin phenomenon Occasionally, related to antibodies Often, related to insulin receptor or post-receptor defects


b. The secondary conditions

Age of onset <30 years old More than 40 years old

Urgent, slow, mild

Weight loss

Incidence rate about 0.2% about 2.0%

Ketosis common rare

Comorbidities are dominated by infections and metabolic disorders.

Blood anti-islet cell antibody multiple positive multiple negative

Oral hypoglycemic drugs are often ineffective and effective

Insulin therapy is required only about 25% of patients


Etiology and Pathogenesis (metabolic disease)

 Diabetes is complex and often causes the onset of multiple factors.

 1. Genetics It is clear that genetic factors affect the onset in some diabetic patients, such as one case of diabetes in twins and the other 50% of cases. In the case of monozygotic twins, they usually occur at the same time. According to statistics, if the father or mother suffers from non-insulin-dependent diabetes, the risk of developing children is about 10-5%. If both parents have non-insulin-dependent diabetes, the risk of developing children is higher. If one brother develops non-insulin-dependent diabetes, the risk of other brothers is 10-15%. However, the incidence of non-insulin-dependent diabetes in children of insulin-dependent diabetes is not higher than that of the general population.


It has been confirmed that insulin-dependent diabetes mellitus is associated with a specific HLA, and those at high risk are DR3, DR4, DW3, DW4, B8, B15 and so on.


At present, most people think that some diabetes is a multi-gene genetic disease, not determined by a certain gene, but that the disease may occur when the amount of genes reaches or exceeds its threshold.


2. Viral infection Many diabetes occur after viral infection, such as rubella virus, mumps virus, coxsackie virus, adenovirus, etc., which may be related to viral pancreatitis. Of course, diabetes occurs in every case of viral infection.


3. Anti-islet β-cell antibodies were found in the serum of some diabetic patients who were immunized at home. Injection of anti-islet β-cell antibodies to experimental animals can cause abnormal glucose tolerance. Pathological examination can also see the infiltration of lymphocytes and eosinophils in islets . It has also been reported that the use of immunosuppressive therapy in the early stages of onset of insulin-dependent diabetes can achieve good results and even “cure.”


4. Secondary diabetes, such as the destruction of most of the pancreatic islet tissue and pancreatic fiber bundles, hyperadrenal cortex function, functional pituitary adenoma, pheochromocytoma, etc. can cause secondary diabetes, that is, symptomatic diabetes. Long-term use of dihydrogram urine plugs, corticosteroids, adrenergic drugs, etc. may cause or promote the exacerbation of diabetes. Certain hereditary diseases such as Turner syndrome are also prone to diabetes.


5. Other incentives

 (1) Eating habits: There is no obvious relationship between high-carbohydrate diet and food composition. For example, refined food and sucrose can increase the incidence of diabetes. According to epidemiological analysis, high protein diet and high fat diet may be more important risk factors.


(II) Obesity is mainly related to the occurrence of non-insulin-dependent diabetes. Obesity is caused by the calories of food exceeding the body’s needs. Excessive eating can cause hyperinsulinemia, and the number of insulin receptors in obese people decreases, which may induce diabetes.


Pathology (Metabolic Disease)

The number of islet β cells was reduced, the nucleus was deeply stained, and the cytoplasm was scarcely degranulated. Alpha cells are relatively increased, fibrous tissues adjacent to the capillaries in the pancreatic islets, extensive fibrosis, thickening of the intima of the blood vessels, and pancreatic islet pathological changes in insulin-dependent diabetic patients are often obvious. The number of beta cells can be only 10% of normal. Insulin-dependent diabetes mellitus is relatively mild. About one third of the cases have no histologically positive lesions under the light microscope. In the early stages of insulin-dependent diabetes, lymphocytes and mononuclear cells were seen in the islets and around them. Nuclear cell infiltration is called “isletitis.”


About 70% of diabetic patients have lesions in small blood vessels and microvessels, which are called diabetic microangiopathy. Common in the retina, kidney, heart muscle, muscle, nerve, skin and other tissues. The basic lesion is that the PAS-positive substance deposits under the endothelium and causes microvascular basement membrane enlargement. This lesion has high specificity. The large and middle arteries of the diabetic patient include cerebral arteries, vertebral arteries, renal arteries, and epicardial arteries. Non-diabetics are also seen in the same lesions, so they lack specificity.


Diabetic neuropathy is more common in patients with a longer course and poorly controlled disease. Axial degeneration of the nerve fibers at the end, followed by segmental diffuse demyelinating changes, and microhematopathy in neurotrophic blood vessels can occur. The lesions sometimes involve nerves. Root, paravertebral sympathetic ganglia, spinal cord, cranial nerve and brain parenchyma, infection nerve damage is more obvious than motor nerve damage.


Liver steatosis and degeneration, in severe cases, changes similar to cirrhosis. Myocardium swelled from turbidity and degeneration to diffuse fibrosis.


Clinical manifestations of Non insulin dependent metabolic disease

 People with early non-insulin-dependent diabetes are asymptomatic and more likely to be found during health checks, censuses, or other diseases. According to WHO statistics from Japan, about 25% of newly diagnosed diabetics have kidney function changes. This indicates that it is not a stage A case. According to the World Health Organization-funded census in Daqing, Northeast China, and review data after 3 years, about 80% of diabetic patients were not detected and processed before the census.


I. Insulin-dependent diabetes has an acute onset, often with sudden polyuria, polydipsia, polyphagia, and weight loss. There are obvious hypoinsulinemia and hyperglycemia, clinical susceptibility to ketoacidosis, and various acute and chronic infections. Some patients have large blood sugar fluctuations, often with high blood sugar and low blood sugar, which is difficult to treat, which is the so-called fragile diabetes in the past. Many patients can suddenly relieve symptoms, and some patients also restore endogenous insulin secretion, and it is not necessary and only requires a small dose of islet gauze treatment. The remission period can last for several months to 2 years. Intensive treatment can promote remission. Insulin therapy is still needed after relapse.


II. Non-insulin-dependent diabetes polyuria and polydipsia are lighter, there is no significant overeating, but fatigue, fatigue, and weight loss. Patients often come for treatment with chronic comorbidities, such as vision loss, blindness, numbness, pain, anterior heart pain, heart failure, renal failure, etc., more patients are found during health examinations or other diseases .


III. The clinical manifestations of primary diabetes are mostly the primary symptoms.


IV. Clinical manifestations of chronic comorbidities

 (1) The change of cardiovascular disease: Diabetic heart disease is characterized by typical angina pectoris (long duration, mild pain, ineffective coronary expansion drugs), and myocardial infarction is mostly painless and refractory heart failure. Limb gangrene. The incidence of cerebrovascular disease is also high, which is an important factor in the death of diabetes.


(2) Renal lesions: Due to the thickening of the glomerular system and basement, the early glomerular filtration rate and blood flow increase, and then gradually decrease significantly. Intermittent proteinuria occurs and is found to be persistent proteinuria, hypoalbuminemia, edema, azotemia, and renal failure. The normal renal glucose threshold is to ensure that the blood glucose does not rise seriously. If the blood glucose often exceeds 28mmol / L (504mg / dL), it indicates that there must be permanent or temporary kidney damage. Under current conditions, the progressive kidney disease is Difficult to reverse.


(3) Neuropathy is more common in middle-aged patients and accounts for about 4-6% of the diabetic population. Using electrophysiology examination, it can be found that more than 60% of diabetic patients have different degrees of neurological disease. Clinically, peripheral neuropathy (including sensory nerves, motor nerves, and autonomic nerves) and spinal cord disease (including spinal muscular atrophy, pseudospinalis, amyotrophic lateral sclerosis syndrome; posterior lateral sclerosis syndrome, spinal cord softening, etc. ), Brain lesions (such as cerebrovascular disease, cerebral softening, etc.). Timely and effective treatment of diabetes often has a good effect on neuropathy, but sometimes, even when the diabetes control is satisfactory, diabetic neuropathy may still occur and develop.


(4) Ocular complications are more common, especially those with a disease course of more than 10 years, the incidence rate is more than 50%, and more serious, such as retinopathy of microhemangioma, bleeding, exudation, neovascularization, organogenesis, retina Exfoliation and vitreous hemorrhage. Others include conjunctival vascular changes, irisitis, iris roseola, regulating muscle paralysis, low intraocular pressure, hemorrhagic glaucoma, cataracts, transient refractive abnormalities, optic neuropathy, and extraocular muscle paralysis. The patient progressed rapidly and became blind in the short term. Good control of diabetes may delay the occurrence and development of ocular comorbidities.


(5) Other hypoxic tissues cause subcutaneous blood vessels to dilate due to hypoxia and cause complexion. Due to arteriolar and microvascular disease, subcutaneous bleeding and bruising are often present. Purpura and ischemic ulcers can occur in poor blood supply sites, with severe pain, which is more common in the feet. Neurological dystrophy can also affect the joints, which are Charcot joints, which occur in various joints of the lower limbs. The affected joints can have extensive bone destruction and deformities.


Laboratory Inspection (Metabolic Disease)

 1. Glucose arterial blood, microvascular blood and venous blood glucose levels have a difference of 0-1.1mmul / L (0-20mg), which is more obvious after meals, and generally venous blood shall prevail. Because the glucose level in red blood cells is low, the whole blood glucose value is about 15% lower than the plasma or serum glucose value. The specific glucose oxidase method is reliable for this metabolic disease.

The normal glucose concentration in fasting venous blood is 3.9-6.1mmol / L (70-110mg / dl). In the past, the reduction method was used for measurement. Since blood contains a non-constant non-glucose reducing substance, the value of the measurement result is high. Glucose oxidase in blood can reduce blood glucose concentration by about 0.9mmol / L (17mg / dl) per hour at room temperature, so specimens should be measured immediately after blood collection or made into protein-free solution and stored at low temperature.


Fasting blood glucose if the insulin secretion ability is not less than 25% of normal, and most of the fasting blood glucose is normal or slightly elevated, so multiple fasting blood glucose higher than 7.7mmol / L (140mg / dL) can diagnose diabetes, but normal fasting blood glucose cannot Eliminate diabetes.


2 hours postprandial blood glucose is generally used to monitor the control of diabetes. If it is higher than 11.1mmol / L (200mg / dl), diabetes can be diagnosed. If only 9.5mmol / L (190mg / dl) is used, a glucose tolerance test should be performed to confirm the diagnosis in this metabolic disease.


2. The normal person’s renal glucose threshold is about 8.9mmol / L (160mg / dl) in this metabolic disease, but there are individual differences, only positive urine glucose can not be diagnosed with diabetes. Fasting urine glucose is often negative in non-insulin-dependent diabetic patients. Therefore, for preliminary screening of diabetes, urine glucose should be measured 3 hours after meals. If the reduction method is used, false positives should be noted, for example, after taking salicylates, chloral hydrate, vitamin C and other drugs.


3. The glucose tolerance test oral method (CGTT) is an important method for the diagnosis of diabetes. The regular test procedure is to measure fasting blood glucose first, and then take 75 g of oral glucose (1.75 g / kg under 12 years), and 1, 2, 3 hours after taking sugar. Repeat the blood glucose measurement. According to the World Health Organization Diabetes Expert Committee, diabetes can be diagnosed at any time with blood glucose ≥ 11.1 mmol / L (200 mg / dL) and / or fasting blood glucose ≥ 7.8 mmol / L (140 mg / dl). In order to have a reliable glucose tolerance test result, it should be noted that:

i. Fasting must be performed for 10-16 hours before the test.

ii. You must eat appropriate calories and carbohydrates a week before the test.

iii. The test should be performed between 7-11 am.

iv. Smoking, alcohol, coffee and excitatory drugs should be started at least 8 hours before the test.

v. Try to rest as quietly as possible during the test.

vi. Prohibit drugs that affect glucose metabolism.

vii. A variety of acute and chronic diseases have different degrees of influence, which must be considered when judging the measurement results. After taking glucose, the arterial blood glucose rises faster than the venous blood sugar and recovers slowly. After about 3 hours, the arterial and venous blood sugar gradually become consistent.



Blood glucose value mmol / L (mg / dl)

Venous blood


Fasting ≥6.7 (120) ≥7.8 (140)

2 hours after glucose load ≥10.0 (180) ≥11.1 (00)

Impaired glucose tolerance

Fasting < 6.7 (120) < 7.8 (140)

2 hours after glucose load ≥6.7 (1200- <10.0 (180) ≥7.8 (140) - <11.1 (200)


The intravenous glucose tolerance test (IVGTT) is a non-physiological test method, so it is generally not used except for those with severe gastrointestinal dysfunction. Method: 50% grape juice at 0.5g / kg dose in 2-4 minutes The intravenous injection is complete. If the venous blood glucose does not fall to the normal range within two hours, impaired glucose tolerance is indicated.


4. Glycated protein measurement includes glycated hemoglobin and glycated albumin, etc., which directly reflects the occurrence of chronic comorbidities, and its significance is more than multiple consecutive blood glucose measurements. Widely used in diagnostic and therapeutic monitoring. Glycated hemoglobin showed an average blood glucose condition of 3 months, and glycated serum protein showed an average blood condition of 3 weeks.


5. The insulin release test procedure and precautions are the same as the glucose tolerance test. The purpose is to understand the ability of pancreatic beta cells to respond to glucose load. Insulin-dependent diabetes mellitus has a low fasting insulin level and a weak response after glucose load. The increase in peak value does not exceed the fasting value. 2.5 times. Fasting insulin levels in non-insulin-dependent diabetes mellitus are low, normal, or even high.

The peak insulin peak after glucose load exceeds 2.5 times the fasting value, but its appearance is delayed, mostly after 2 hours. Its insulin secretion peak composition is mainly proinsulin, and its biological activity is not high. Insulin release tests are instructive in determining treatment options. Due to the large amount of variation in C-peptide determination, its practical application is limited.


6. For other metabolic disorders, blood lipid, blood gas analysis, blood urea nitrogen, creatinine, uric acid, lactic acid, β2 microglobulin, and hemorheology should be measured.


Diagnosis and Differential Diagnosis

According to the medical history, various chronic complications and laboratory tests are not difficult to diagnose. The following diseases should be identified.


First, the renal glucose threshold caused by too low renal glucose threshold, characterized by urine glucose positive but not accompanied by hyperglycemia, and no significant energy metabolism disorders or disorders. About 1% of urine glucose positive. Most are inherited genetic disorders, and may have amino acid urine. Diabetes can also occur when hepatolenticular degeneration, poisoning of certain heavy metals (such as tin, cadmium, uranium, etc.), and renal tubular damage caused by lysosulfate and nifediene.


Second, nourishing diabetes in a small number of “healthy people”, patients with hyperthyroidism, liver disease, gastrointestinal short-circuit patients, after eating a lot of carbohydrates, especially monosaccharides and disaccharides, due to excessive absorption, there may be transient Diabetes. The differential diagnosis with diabetes is that the fasting blood glucose is normal in the glucose tolerance test, and the blood glucose concentration is higher than normal in half an hour and one hour, but normal after two hours.


Third, other diabetic urine is mostly congenital abnormalities or excessive consumption of fructose or galactose, which can cause fructose urine or galactose sugar urine, the reduction of urine sugar test was positive, and grape oxidase method was negative.


Treatment of this Metabolic Disease

I. Purpose Under the current conditions, diabetes is basically incurable. The purpose of treatment is to maintain as long as possible no complications and a relatively normal life. For this reason, in addition to trying to maintain blood glucose in the normal range throughout the time, and should restore the metabolic pathways to normal. The basic criteria for a well-controlled condition are normal or near normal fasting and postprandial blood glucose, normal glycated hemoglobin and glycated serum protein, normal blood lipids, normal hemorheology, no acute metabolic comorbidities and stable weight. Maintain a more normal living and working ability.


II. General treatment Educates patients to correctly understand and treat the disease, and actively cooperate with treatment. Most people with early diabetes have no obvious clinical symptoms. Therefore, the urgency of treatment is not felt, and it is unwilling to adhere to treatment. However, if chronic comorbidities occur, it will be irreversible and even difficult to control its development. Therefore, it is necessary to educate patients to understand the importance of adherence to treatment in the early stages of disease.


Teach patients to master self-monitoring methods to properly adjust their diet and medication. Will deal with adverse reactions to the drug. Such as hypoglycemia response, so that patients can self-regulate and treat under the guidance of a doctor, in order to strive for better prognosis.


III. Diabetes control diet requires the same amount of calories and nutrition as normal people. However, due to metabolic disorders and disorders of the body’s regulation mechanism, people with diabetes need to rely on artificial in vitro regulation. Therefore, they should be given a constant diet and relatively constant drugs to maintain metabolism. The normal progress and stability of the internal environment.


(1) Total calories The total daily calories required is related to weight and work nature. However, individual differences are very large. It is necessary to keep the weight stable in the ideal range and maintain normal work and living capacity. Accurate, regular inspections and timely adjustments.


Relationship between total food calories (KJ / Kg-d) and body size in people with diabetes


[BMI] = Weight (Kg) / Height (M) 2]


Heavy physical labor moderate physical labor light physical labor bed rest

Weight loss (BMI <20) 188 ~ 209 167 146 83 ~ 104

Normal (BMI20 ~ 25) 167 146 125 62 ~ 83

Obesity (BMI > 25) 146 125 83 ~ 104 62


The table shows the total calories required for men with diabetes, which is reduced by 10% for women. Patients over 55 years of age have reduced their total calories by 10-25% due to reduced physical activity. The main factors for the final adjustment are the changes in weight and physical strength.


(2) Carbohydrate should account for about 65% of total calories, avoid monosaccharides and disaccharides, and should contain 8-10 g / d of various polysaccharides. The excessively fast absorption of carbohydrate blood sugar peaks appear early and concentrated, which is not conducive to control, and the absorption is too slow, especially for people with diabetes. The gastric emptying time is prolonged, which will increase the late blood sugar after meals. You can use morpholine or Cisaprid to promote gastric excretion Empty, and use longer-acting hypoglycemic drugs. If the carbohydrate in the diet is too low, it will reduce the reserve function of islet β cells, which is not good for patients.


(3) The protein content should be about 0.7g / kg / d. Although diabetic patients tend to have a negative nitrogen balance and protein is often lost from the kidneys, if a large amount of protein is added to the food, it will damage the kidneys, which is very unfavorable. Therefore, people with early diabetes should pay attention to control the protein in food, even when the kidney loses a large amount of protein, it should also be careful to supplement the excess protein. It should be based on animal proteins. Because the proportion of amino acids in plants is not exactly the same as the protein required by the body, incomplete utilization and the elimination of waste will increase the burden on the body, especially the kidneys, which is harmful and unprofitable.


(4) Except for carbohydrates and protein, all fats and fats are provided by fat. Chinese people have a diet of about 0.5kg / kg / d, and there is a tendency for ketogenic too much fat. Due to metabolic disorders and poor self-regulation, fat should contain more than 25% of unsaturated fatty acids in total, and cholesterol should be reduced as much as possible.


(5) The dietary counting method has previously advocated a precise calculation of food composition. The heat production per g of carbohydrates and proteins is approximately 16.7Kj (4.5 kcal, and the heat production per g of fat is approximately 32.6Kj (9.0 kcal). According to the table of food ingredients Calculate the daily food composition. This method is more scientific, but there are still many shortcomings, such as rich and strong flour, standard flour are flour, but the composition is very different, and the place of origin is also different. The same is the carbohydrate. Sugar, sugar cane is mainly sucrose, and its impact on diabetes is completely different.

In addition, even if the patient is a scientific worker, it is not possible to strictly measure and execute it every day. Generally, the staple food is basically fixed according to the calculation, and the food is adjusted after the relative stability, so that The food varieties are full of changes to meet the requirements of life, and are regularly adjusted based on changes in blood sugar, urine glucose, weight, and working and living ability.


Many countries use local foods to compile food swap tables. Stevia can be used as a sweetener, and saccharin is not easy to overdo it. thus, this is very helpful in this metabolic disease.


It should be noted that the diet and raw foods of the ethnic group are appropriate in this metabolic disease. You can eat fruits that are not rich in monosaccharides or disaccharides but rich in pectin, such as apples and pears, but not in excess.


IV. Oral hypoglycemic drugs: In this metabolic disease oral hypoglycemic drugs can be used when people with type diabetes simply cannot control their blood glucose and metabolic pathways effectively, especially those whose blood sugar is often lower than 13.9mmol / L (250mg / dl). Some people claim that it can be combined with insulin therapy.

If one oral hypoglycemic drug is ineffective or ineffective, try another one, which may be effective. Oral hypoglycemic drugs have secondary failure due to various reasons after being taken for months or years, and should be replaced with other oral hypoglycemic drugs. In type 2 diabetes, about 10-20% are ineffective for oral hypoglycemic drugs and need to be treated with insulin. There are two common types of oral and blood glucose medications:


(1) Sulfonylureas, hypoglycemic drugs in this metabolic disease are sulfonylurea compounds that can promote the secretion of pancreatic islets by pancreatic islet β cells. In addition, they reduce blood glucose by affecting pathways outside the islets such as receptors and post-receptor processes. Improper use may result in death from cardiac accidents and hypoglycemia.


Indications of this metabolic disease:

i. Most type diabetes (metabolic disease)

ii. Those with normal weight or low body weight

iii. Still maintain a certain islet β cell function.

Non-indications or contraindications


i. Type I diabetes

ii. Complicated with acute metabolic disorders such as ketoacidosis, lactic acidosis, non-ketogenic hyperosmolar coma, etc.

iii. Severe infection, trauma, surgery and other stress conditions

iv. severe liver , Renal insufficiency, affecting pharmacokinetics

v. during pregnancy (with the risk of teratogenicity and hypoglycemia in the fetus and newborn).


Side effects include:

i. hypoglycemia, slower onset than insulin, but the duration can be as long as 1-5 days, which can lead to death

ii. secondary failure, mostly appear after 1 to several years of medication. Switching to its sulfonylurea drugs may still be effective iii. a few patients have gastrointestinal reactions and allergic reactions such as rashes

iv. occasional bone marrow suppression.


Commonly used oral hypoglycemic drugs are:

i. excellent hypoglycemic, which is characterized by a strong effect, mainly affecting the β phase of insulin secretion. The absorption is about 40%, the peak time of blood is 2-4 hours, and the average half-time of blood is 4.8 hours. The dose is 2.5-15mg / d for this metabolic disease.

ii. Promethazine (special secretion of pancreas), strong effect, more common hypoglycemic response. Due to the long action time, accumulation may occur. The strongest time is 8-10 hours, the blood half-life is 30-36 hours, the duration of the effect is 22-65 hours, and 100% is excreted by the kidneys within 10-14 days. The dosage is 250-500mg, which is taken orally once every morning.

iii. There can be oral hypoglycemic drugs in the market thatare suitable for patients with renal dysfunction. The strongest time is 2-3 hours. The main side effects are in addition to allergic dermatitis and hypoglycemia, and there is a risk of teratogenicity, so pregnant women are prohibited. Due to the impact of stress and concentration, it cannot be used by practitioners such as car drivers. The commonly used dose is 45-90mg / d, up to 120mg / d, taken in divided doses.

iv. These drugs mainly acts on the α-phase of insulin secretion, and the extraislet effect is more obvious, and the anticoagulant effect is stronger. The strongest action time is 2-6 hours, and the action duration is 24 hours, which is mainly excreted by the kidneys. The dose is 40-320mg / d, taken in the morning and noon. Hypoglycemia is rare and mild.

v. In addition to the effects of β-cells on mepitah (menida), the extra-islet effect is strong. There is no accumulation, and the response to hypoglycemia is relatively short. Can inhibit platelet aggregation and have fibrinolytic effect. The strongest action time was 1-2.5 hours, and 97% was excreted by the kidneys in the first day. Side effects In addition to the aforementioned, occasional headaches, dizziness, fatigue, etc., the dose of 5-30 mg / d, orally taken 1 to 3 times.

vi. Glucose, in addition to increasing the amount of insulin secretion, can reduce glucagon secretion, improve microcirculation, reduce red blood cell adhesion, etc., the absorption is about 95%. The side effects are the same as before, which can cause weight gain, but the hypoglycemic response is light. The dose is 12.5-100mg / d, which is taken orally every morning, and if necessary, 12.5-37.5mg is taken before lunch.


(B) The mechanism of action of biguanide hypoglycemic drugs is not completely clear. It is known that it can reduce the absorption of glucose, promote glucose hydrolysis and enhance the effect of insulin. Due to its high side-effect (lactic acidosis), it has a high mortality rate and cannot make glucose metabolism pathways. It returned to normal, so it has been banned in some countries. The domestic use of phenformin (glycemic) is 25-150mg / d, which is broken down by the liver, and the effect lasts 8-12 hours.


People with type 2 diabetes, especially obese people may have adjuvant treatment for people with type 1 diabetes, non-indications or contraindications: 

i. severe liver and kidney dysfunction with acute metabolic comorbidities such as ketosis Acidosis, lactic acidosis, non-ketogenic hypertonic coma, etc.

ii. Patients with hypoxia, such as heart failure, emphysema, shock, etc.

iii. Patients with severe infection, trauma, surgery and other stress states.

iv. Pregnancy.


Side effects:

i. Prone to lactic acidosis in the elderly and renal dysfunction.

ii. Gastrointestinal reactions such as loss of appetite, nausea, vomiting, abdominal pain, diarrhea and so on.

iii. Some patients feel burnout, fatigue, weight loss, headache, dizziness, etc. after taking it for a long time.

iv. Cardiovascular mortality is high.


V. Insulin therapy Insulin can be divided into different types according to the duration of action.

Insulin doses must be individualized, and the differences can vary widely. Adjusted approximately every 3-5 days. At the beginning, ordinary insulin is about 20u / d, and it is injected three times before meals. Patients with a stable renal glucose threshold can estimate the insulin dose before urinary glucose positive meals. Approximately 4u insulin is used for each “+”, and adjustments will be made according to the effect. In order to prevent postprandial hyperglycemia, subcutaneous injection is usually performed 15-45 minutes before each meal. If the patient’s islet function is poor and basal insulin secretion cannot be maintained, long-acting insulin should be added or insulin should be added again 10-10 minutes later injection. To keep the blood glucose in the normal range at dawn.


Recently, high-purity single-peak insulin and semi-synthetic human insulin are used to reduce anti-insulin antibodies, and the action time is slightly earlier than ordinary insulin. Changing the order of amino acids in the insulin peptide chain to make super fast-acting insulin can be injected after a meal. The dosage can be flexibly controlled according to the amount of meals. You can also change the isoelectric point of insulin by changing the amino acid sequence and delay absorption, that is, stable long-acting islets without additional proteins. In addition, there are insulin nasal drops in foreign countries, and the absorption is not stable.


Several insulin preparations and their action time


Action Category Injection




Action time * (hours)

Injection time

Start strongest last

Fast-acting regular (regular) insulin


(Regular insulin)






1/2 ~ 1



2 ~ 4



6 ~ 8

Depending on the condition, 1/2 hour before meals, 3 to 4 times a day

Zinc crystalline insulin


(Crystallini zincinsulin)






1/2 ~ 1



4 ~ 6



6 ~ 8

Depending on the condition, 1/2 hour before meals, 3 to 4 times a day

Semi-slow insulin zinc suspension


(Semlentc insalin)

Subcutaneous 1 ~ 2 4 ~ 6 12 ~ 16 Same as above, 2 ~ 3 times a day

Medium-acting slow insulin zinc suspension


(Lentc insulin)

Under the skin 2 ~ 3 8 ~ 12 18 ~ 24 1 hour before breakfast (dinner), 1 or 2 times a day

Neutral protamine zinc insulin


(Neutral protamine Hagedone, NPH)

Subcutaneous 3 ~ 4 8 ~ 12 18 ~ 24 Same as above

Long-acting extra-slow insulin zinc suspension


(Ultralente insulin)

Under the skin 5 ~ 7 16 ~ 18 30 ~ 36 Breakfast or dinner 1 hour, once a day

Protamine zinc insulin


(Protamine zinc insulin)

Subcutaneous 3 ~ 4 14 ~ 20 24 ~ 36 Same as above


* The action time is for reference only, and varies due to many factors such as insulin absorption and degradation.


For intractable patients, continuous subcutaneous insulin infusion can be treated with an adjustable insulin pump, which has certain effects. Continuous artificial islet therapy has better results, especially for continuous use for more than 3 years.


Indications for insulin therapy for his Metabolic Disease:

i. All type 1 diabetes.

ii. Poorly controlled by other therapies in people with type II diabetes.

iii. There are acute metabolic comorbidities such as ketoacidosis, lactic acidosis and non-ketotic hypertonic coma.

iv. Under stress such as severe infection, trauma and surgery.

v. combined pregnancy.

vi. A variety of reasons affect people who eat, not suitable for indications: Hyperinsulinemia can promote arteriosclerosis, and should not be treated with insulin.


Side effects:

i. Hypoglycemia. Attacks are more acute, such as coma lasting more than 6 hours may cause central irreversible damage.

ii. Allergic reactions, mainly injection local pain, induration, rash, and occasional systemic allergic reactions such as urticaria, purpura, serum disease, localized edema, bronchospasm, collapse, gastrointestinal reactions such as acute pulmonary edema. More common when injecting preparations containing additional protein. 

iii.The injection area cures subcutaneous fat malnutrition.

iv. Insulin antagonism or insulin resistance diabetes. Drug resistance is defined as a daily insulin requirement of more than 200u for more than 48 hours. The incidence is 0.1-3.6%.

v. Contradictions in treatment. For some chronically uncontrolled diabetic patients, if intensive control is achieved in a short period of time, a variety of long-term comorbidities will significantly worsen in half a year.


There are two phenomena that must be understood in the treatment of diabetes:

i. Morning phenomenon, blood glucose is basically stable before 3-5 am, but there is no incentive to rise blood glucose up to 1.1mmol / L (20mg / dL) above 6-8. Morning phenomenon may be related to changes in insulin receptors.

ii. Hyperglycemia after hypoglycemia, conscious or unconscious hypoglycemia response and hypoglycemic coma, can cause reactive hyperglycemia, which lasts for several hours to several days. Hypoglycemia occurs at night also known as the Somogyl effect.



Effective treatment was started early, and the prognosis was good. The main causes of death were cardiovascular, brain, and renal complications. The incidence of malignant tumors was also higher than the population. Patients found after the age of 60 had a poor prognosis.


Prevention from this Metabolic Disease

On weekdays, natural foods and rough processed foods are the mainstays, and it is advisable to use the national diet. Should contain the right amount of glycans. Although there is no sufficient evidence to prove that large amounts of monosaccharides and disaccharides can cause diabetes. However, it is clear that it is not beneficial to health. Proper physical activity is necessary. Regular and proper health check-ups are found in time. Early and correct treatment is a prerequisite for a good prognosis.


Section 3 Diabetic ketoacidosis

Acute metabolic comorbidity due to the accumulation of organic acids and ketone bodies in carbohydrate, protein and fat metabolism disorders when diabetic patients are severely lack of effective insulin.



Regardless of various inducements that exacerbate diabetes, due to severe insulin deficiency, the effects of hormones, such as glucagon, catecholamines, growth hormone, and adrenal corticosteroids, which are opposite to insulin, are more significant on metabolism. Accelerate fat decomposition, and increase the amount of ketone bodies produced by beta oxidation of fatty acids in the liver. As the sugar has no xenobiotics, the tricarboxylic acid cycle stagnates, blood sugar rises, and ketone bodies accumulate. When ketone body production is greater than tissue utilization and renal excretion, the blood ketone body concentration can reach 50-300mg / dl (normal value is 1.0mg / dL). The total daily urinary ketone body of normal people is 100mg, and that of diabetic patients is about 1g / d.

When ketoacidosis occurs, up to 40g / d can be excreted. When combined with renal dysfunction, ketone bodies cannot be excreted from the urine, so although ketoacidosis occurs, urine ketone bodies are negative or only trace amounts. Due to the accumulation of a large amount of organic acids, the thoracic storage in the body is consumed, and the compensatory capacity of the body fluid buffer system and the respiratory system is exceeded, that is, acidosis occurs, and the arterial blood PH value can be lower than 7.0. Due to the increase in urine osmotic pressure, a large amount of water, sodium, potassium, and chlorine are lost, which can reach 10-15% of total body fluids.



It is more common to inappropriately interrupt insulin therapy, especially when patients are under stress. It is also seen in newly diagnosed diabetic patients without proper treatment, who complain of coma with ketoacidosis. Can also be induced by mental factors.


Clinical Manifestations

1. The symptoms of diabetes worsen. Thirst, increased urine output, fatigue, etc., but there is no obvious overeating.


2. Digestive system symptoms Appetite loss, nausea, vomiting, vomiting can also occur after drinking water.


3. Symptoms of Respiratory System Breathing is deep and fast when tartarosis occurs, showing Kussmonl breathing. When the pH of arterial blood is lower than 7.0, breathing becomes shallower and slower due to respiratory central paralysis and muscle weakness. The exhaled breath may have an acetone smell (rotten apple smell).


4. Dehydration: When the amount of dehydration exceeds 5% of body weight, the amount of urine decreases, the skin and mucous membranes dry, and the eyeballs sink. If the amount of dehydration reaches more than 15% of body weight, due to reduced blood volume, circulatory failure, rapid heart rate, decreased blood pressure, cold limbs, and no significant increase in body temperature even with concurrent infection.


5. There are obvious individual differences in mental state, dizziness, headache and mental atrophy in the early stage. Gradual drowsiness, irritability, dullness, tendon reflexes disappear, and to coma, pathological reflexes often occur.


6. Others Extensive and severe abdominal pain, abdominal muscle tension, and occasional rebound pain, often misdiagnosed as acute abdomen. Refractive errors can occur due to dehydration.


Diagnosis of this metabolic disease

First, blood glucose in patients without treatment is mostly moderately elevated. If the blood glucose exceeds 33.3mmol / L (600mg / dL), it indicates that there is renal dysfunction. People with incorrect treatment (such as high-dose insulin injections) may develop hypoglycemia and ketosis is not corrected.


Second, when the ketone body has clinical ketosis, the blood ketone body rises above 5-10 times. Urine ketone body measurement method is simple, except for those with severe renal dysfunction, which are parallel to clinical manifestations, and can be used as a diagnostic basis.


Third, the arterial blood PH value Early in ketosis due to the buffer system of body fluids and the role of lungs and kidneys, blood PH value can be maintained in the normal range. But the carbonate and tritium decreased significantly. If the increase in H + exceeds the body’s buffering capacity, the blood pH will drop sharply. The binding capacity of CO2 only reflects the storage condition of radon and cannot directly reflect the blood PH value.


The above three tests can confirm the diagnosis of diabetic ketoacidosis, but there are some changes that must be paid attention to. The uric acid excreted by the kidney is reduced during ketosis, and transient hyperuricemia can occur. The blood sodium and potassium concentrations are mostly in the normal range, even higher, and the body has lost a large amount of sodium, potassium, and chlorine, and the total number of white blood cells and granulocytes can be significantly increased even without infection.


Differential Diagnosis of this metabolic disease

Differential diagnosis in this metabolic disease: It should be distinguished from other diabetic coma, such as hypoglycemic coma, lactic acidosis, non-ketotic hyperosmolar coma, etc. For mild disease, it should be distinguished from starvation ketosis, which is mainly seen in patients with more severe nausea and vomiting, who cannot eat, such as severe pregnancy vomiting, which is characterized by normal or low blood sugar, ketosis, but more acidosis serious.


Treatment of this metabolic disease

1. After dehydration diagnosis is clear, dehydration should be corrected as soon as possible. Input 1 liter of fluid within 1-2 hours, and refill 1 liter within 3 hours, until the dehydration is corrected and circulating renal function is maintained to reduce hyperglycemia and ketosis. Acidosis. Generally dehydration is about 10% of body weight. It is advisable to keep the urine volume above 2ml per minute after fluid replacement, and reduce fluid replacement volume and speed appropriately for those with heart disease.

At the beginning, normal saline can be input. When the blood sugar drops to 11.1-16.6mmol / L (200-300mg / dL), 5% glucose solution can be given, and when the blood sugar is lower than 11.1mmol / L (200mg / dL), 10% glucose solution can be given. In order to avoid brain edema, it is not advisable to input too much sodium, hypotonic fluid and make blood sugar fall too fast.


2. Insulin For severe patients, intravenous drip of ordinary insulin can be continued, and 4-8 u / h can effectively inhibit ketone body production and glycogenogenesis, and restore the operation of the tricarboxylic acid cycle. If the dose is too large, the effect will not be achieved faster than the limit of the receptor, and the purpose of early treatment is to eliminate the accumulated ketone body. No advantage, no longer use high-dose insulin treatment. Because the patient is obviously dehydrated, the circulation is poor, the absorption is difficult to control, and subcutaneous injection is prone to dose accumulation, which causes hypoglycemia. To facilitate adjustment, do not use long-acting insulin.


3. Correction of Electrolytic Disorders Although the blood potassium was normal or high at the time of admission, it gradually decreased after 1-4 hours of starting treatment, and potassium chloride or potassium acid buffer solution should be added in time to 30-60 mmol. And often monitor blood potassium and ECG to adjust the dose. Renal insufficiency and low urine output should not be supplemented with large doses of potassium. And the sodium and chlorine balance should be found and corrected in time.


4. Correct the acid and tritium balance imbalance generally do not use drugs, because:

i. ketones are organic acids, can be metabolized and disappear.

ii. Because CO2 is easier to pass through the cell membrane and blood-brain barrier than HCO4, the intracellular and intracranial pH will further decrease after sodium bicarbonate is input.

iii. The blood PH is increased, the affinity of hemoglobin to oxygen is significantly increased, and tissue hypoxia is aggravated.

iv. Increase the incidence of cerebral edema. Therefore, only when the arterial blood PH is less than 7.1, that is, when acidosis is directly life-threatening, 5% sodium bicarbonate solution can be given as appropriate, and the blood PH value ≥7.2 should be stopped. Disable sodium lactate.


Differential diagnosis of diabetic coma

Ketoacidosis Hypoglycemic coma: Hypertonic coma Lactic acidosis

Medical history mostly occurred in adolescents, more history of diabetes, often history of infection, interrupted insulin therapy, etc. History of diabetes, history of insulin injections, oral hypoglycemic drugs, undereating, excessive physical exertion, etc. Mostly occurred in old age, often without diabetes History, history of infection, vomiting, diarrhea, etc. History of liver, kidney dysfunction, hypovolemic shock, heart failure, alcohol consumption, DBI, etc.

Onset and symptoms Slow (2 to 4 days) Anorexia, nausea, vomiting, thirst, polyuria, lethargy, etc. (in hours) Hungry, sweating, palpitations, hand tremors, and other sympathetic nerves. A few days) have drowsiness, hallucinations, tremors, convulsions, etc.


Have anorexia, nausea, lethargy, and symptoms


Skin dehydration, dryness, redness, dampness, sweating, dehydration, dehydration

Breathe deep and fast Normally accelerate deep and fast

Pulse is small, fast and full.

Drop in blood pressure normal or slightly higher drop


Urine sugar positive ++++ negative or + positive ++++ negative or +

Urine Ketone + ~ +++ Negative Negative or + Negative or +

Significantly increased blood glucose, mostly between 16.7 and 33.3mmol / L, markedly reduced <2.8mmol / L, significantly increased, generally above 33.3mmol / L, normal or increased

Significantly increased blood ketone Normal Normal or slightly elevated Normal or slightly elevated

Blood sodium decreased or normal normal normal or significantly increased decreased or normal

PH reduced normal normal or reduced reduced

CO2 binding force reduced normal normal or reduced reduced

Lactic acid slightly increased Normal Normal Significantly increased

Plasma osmotic pressure * Normal or slightly elevated Normal Significantly elevated, often> 350 * Normal


* mmol / L


5. Treatment incentives


6. Artificial islet therapy uses a sensitive sensor that senses blood glucose concentration. After computer information processing, according to the trend of blood glucose concentration change, insulin and / or glucose is injected into the body via a driving device instead of islets to maintain blood glucose balance. For artificial islets. It can adjust the insulin dose instantaneously and instantaneously in two dimensions according to the blood glucose change trend, and can automatically input glucose when necessary, so it is safe and reliable; it can effectively reduce mortality.


7. Others Such as plasma exchange and hemodialysis are limited to severe patients, especially those with more severe renal failure.



The average mortality rate is about 1-15%, which has decreased significantly in the past 10 years. In addition to treatment options, factors affecting prognosis include:

i. Poorer prognosis for patients over 50 years of age.

ii. The coma is deep and the prognosis is long.

iii. The blood glucose, urea nitrogen and plasma osmotic pressure were significantly increased, the prognosis was poor.

iv. Those with severe hypotension have high mortality.

v. Patients with severe complications such as sensation, myocardial infarction, and cerebrovascular disease have a poor prognosis.



Early-onset diabetes, reasonable treatment, can not interrupt islet injection, and properly deal with incentives can effectively prevent or reduce the occurrence of diabetic ketoacidosis.




Section 4: Nonketofie Hyperosmolar Diabetic Coma

Nonketotic hypertonic diabetic coma is clinically characterized by severe hyperglycemia, high osmolarity in plasma, dehydration, and disturbance of consciousness or coma. Rarely, it occurs in elderly patients with diabetes and those with no previous history of diabetes or only mild diabetes without insulin therapy, often with renal insufficiency.



The elderly with cerebrovascular disease and renal dysfunction are prone to central dysfunction of thirst (hypertonic state and severe hyperglycemia also affect the function of central hypothalamus thirst), and renal insufficiency in regulating water, electrolytes, and sugar excretion causes Dehydration, severe hyperglycemia, and some patients have hypernatremia and azotemia.

Induced Factors

Infections, severe burns, hemodialysis, intraperitoneal dialysis, and use of intravenous hypertrophy, diuretics, adrenal corticosteroid preparations, etc.


Clinical Manifestations

Early onset of thirst, polyuria, fatigue, dizziness, loss of appetite, nausea and vomiting. Gradually developed into severe dehydration, limb twitching, delirium, disorientation, irritability or apathy, or even coma. Examination revealed dry skin, reduced elasticity, dry tongue, sunken eyes, decreased blood pressure and even shock. Breathing shallow, heart rate fast. Signs of the nervous system are various. In addition to coma, epilepsy-like seizures, hemiplegia, aphasia, spontaneous muscle contraction, blindness, nystagmus, visual disturbances, positive pathological reflexes, and elevated central body temperature can be present.



The blood glucose increased significantly, more than 33.3mmol / L (600mg / dL), and even as high as 83.3-266.6mmol / L (1500-4800mg / dL). Due to dehydration and renal dysfunction, the renal glucose threshold increased, making blood osmotic pressure More than 320mmol / L (normal value 280-300mmol / L), can be measured directly with an osmometer, or it can be estimated by the following formula.


Plasma osmolality (mmol / L) = 2 × (Sodium + Potassium) (mmol / L) + Blood glucose (mmol / L) + Blood urea nitrogen (mmol / L) or


Plasma osmotic pressure (mmol / L) = 2 × (potassium + sodium) mEd / L + blood glucose (mg / dL) / 18 + blood urea nitrogen (mg / dL) /2.8


Due to severe dehydration and exudation of intracellular fluid, the potassium and sodium concentrations can be normal and high, but the total amount of potassium and sodium in the body is significantly lost. For example, the body’s potassium deficiency can reach 40-100mmol.


Most are accompanied by metabolic acidosis, and the plasma anion is about doubled compared to normal, in this metabolic disease.


Differential Diagnosis

Hypertonic state caused by other reasons, such as dialysis therapy, dehydration treatment, high-dose corticosteroid treatment, etc. can lead to hypertonic state. Patients with a disturbance of consciousness are likely to be misdiagnosed as a cerebrovascular accident and delay treatment. Cerebrovascular accidents commonly used drugs are harmful to the disease, such as mannitol, hypertonic sugar, corticosteroids, etc. all increase the hypertonic state; phenytoin sodium can not stop the seizures and seizures caused by hypertonic state, and can inhibit insulin secretion, Makes hyperglycemia worse. So differential diagnosis is important in this metabolic disease treatment.


First, quickly replenish a large amount of fluid. According to the amount of water loss, about 100ml / kg body weight is required. One third of the total amount should be entered within 4 hours, and the rest should be completed within 12-24 hours. It can be based on central venous pressure and hematocrit. The average volume of urine per minute determines the volume and rate of fluid replacement. The main input is normal saline and 5% glucose solution. Excessive hypotonic solution (0.45% sodium chloride solution and 2.53% glucose solution) may cause cerebral edema, hypovolemic shock, and hemolysis. It must be used with caution. Patients with heart disease should be reduced as appropriate.


Second, insulin treatment is more sensitive to insulin, continuous intravenous drip at a rate of 4-8u per hour, so that blood sugar slowly drops, blood sugar drops too quickly may cause brain edema. Due to insufficient blood volume and poor peripheral circulation, the effective concentration of islets in the blood cannot be stably maintained when subcutaneous injection of insulin, and after circulation is restored, a large amount of insulin enters the blood, which will cause hypoglycemia.


Third, maintain electrolyte balance, timely potassium supplementation, that is, should be sufficient and prevent hyperkalemia, monitoring with blood potassium measurement and ECG examination, especially for those with renal dysfunction and oliguria.


Fourth, treatment incentives Anti-infective treatment, stop all drugs that cause hypertonic state.







Section 5: Diabetic Lacatocidosis (Metabolic disease)

The glucose oxidation process of diabetic patients is blocked, which enhances glucose hydrolysis and produces a large amount of lactic acid, such as insufficient lactate dehydrogenase. Lactic acid cannot continue to oxidize to pyruvate, which makes the synthesis of lactic acid greater than degradation and excretion. An acute metabolic comorbidity of diabetes.



Elderly patients with renal dysfunction or associated hypoxia such as emphysema, pulmonary heart disease, heart failure, shock, and taking biguanide drugs.


Clinical Manifestations

It is more common in elderly diabetic patients. After taking biguanide hypoglycemic drugs, the early manifestations are loss of appetite, nausea, vomiting, rapid breathing, irritability, delirium, and coma.



First of all, it should be distinguished from coma and acidosis. Such as diabetic ketoacidosis, diabetic non-ketogenic hyperosmolar coma, hypoglycemia, etc. It should also be distinguished from the lactic acidosis of its cause.



1. Fluid replacement: For this metabolic disease, in addition to obvious cardiac insufficiency and renal insufficiency, dehydration should be corrected as soon as possible, mainly saline and glucose and sugar.


2. Insulin tincture is continuously infused intravenously at a rate of 0.1u / kg-h to promote the circulation of tricarboxylic acid, which also degrades the acid. The time is long and the amount cannot be large to prevent hypoglycemia in this metabolic disease.

3. The continuous intravenous infusion of vitamin C in large doses is conducive to the oxidation of glucose.

 4. The effect of alkaline fluid is suspicious, and it can make the intracellular fluid and cerebrospinal fluid further acid and induce cerebral edema, which can not reduce the rate. Therefore, it should be used with caution except that poisoning has directly threatened life (blood PH value is lower than 7.1). Sexual liquid.

5. Oxygen absorption: Increase the tissue oxygen supply and promote lactic acid oxidation. The arterial blood oxygen partial pressure of diabetic patients is generally low. Oxygen absorption is helpful to correct lactic acidosis.


6. Hemodialysis or plasma exchange in critically ill patients


7. Treatment incentives to correct hypoxia, stop biguanide drugs, anti-infection and so on, in this metabolic disease.



Because the blood, especially the lactic acid in the brain, cannot be eliminated directly, the curative effect is poor and the mortality is high.





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