Hypoglycemia

Introduction to low blood sugar Hypoglycemic syndrome (hypoglycemic syndrome) is a group of syndromes caused by a variety of causes, blood glucose levels are often lower than 3.36mmol / L (60mg / dl), severe and long-term hypoglycemia can occur extensive neurological damage and concurrency Symptoms, common with functional hypoglycemia and hepatogenic hypoglycemia, followed by insulinoma and other endocrine diseases caused by hypoglycemia, this disease is often misdiagnosed as rickets, epilepsy, mental illness, brain tumors and encephalitis, etc. After proper treatment, the symptoms can be quickly improved. It is very important to identify the disease early, which can achieve the purpose of cure. Delayed diagnosis and treatment will cause permanent neuropathy and irreversible, and the consequences are not good. basic knowledge The proportion of illness: 0.1% (10% probability of illness over 50 years old) Susceptible population: Those who have blood glucose levels below the normal range. Mode of infection: non-infectious Complications: cerebral edema, dementia, coma, shock

Cause of hypoglycemia

First, the cause of the disease

insulin:

Excessive insulin injection or too little food intake after injection, the amount of activity is relatively excessive, can produce a typical acute hypoglycemic response.

Sulfonylureas:

The extent to which these drugs cause hypoglycemia is related to drug half-life, metabolic rate, and the like. When patients have diet reduction, liver and kidney disease, and adrenal insufficiency, they should be alert to the possibility of hypoglycemia.

Ethanol:

Hypoglycemia can occur when drinking a large amount of alcohol continuously and when other foods are ingested less. If you drink a lot of alcohol in the long-term hunger state, you may even die due to severe hypoglycemia.

other:

High doses of vinegar salicylic acid in diabetic patients and normal subjects can lower blood sugar. Hypoglycemia can also occur with propranolol and other B-blockers, and those who receive insulin therapy are more likely to cause severe hypoglycemia. Drugs that can induce hypoglycemia include barbital, pentamidine, methicillin, tetracycline, fluridine, thalidomide, PAS, and BAL. In addition, substances that are toxic to the liver, such as chloroform, cinchon, paracetamol, urethane, neodymium vanamin, and insecticide 1605, can cause hypoglycemia.

There are many causes of hypoglycemia. According to statistics, there are as many as 100 diseases. In recent years, other causes are still found. This disease can be roughly divided into organic hypoglycemia. (The islet and extra-pancreatic primary lesions cause insulin, C-peptide or "Insulin-like substance secretion"; functional hypoglycemia (refers to patients without primary lesions, but due to nutritional and pharmaceutical factors); reactive hypoglycemia (referring to patients with autonomic dysfunction, vagus nerve Excitement, resulting in a corresponding increase in insulin secretion, resulting in clinical hypoglycemia).

In 10314 autopsy tests, 44 cases (0.4%) were confirmed to be insulinomas. The blood glucose of normal people was regulated by many factors, such as central nervous system, endocrine gland, liver, gastrointestinal, nutrition, and exercise. Glucosin, adrenaline, adrenocortical hormone, growth hormone, thyroxine and some gastrointestinal hormones, hypoglycemic hormone only insulin and C peptide, blood sugar rise and fall can also be affected by many physiological factors, such as fasting 48 ~ 72h, Strenuous exercise, drinking, breastfeeding can cause hypoglycemia, neonatal and elderly blood sugar is often low, low blood sugar can also be caused by long-term sugar intake or malabsorption, reduced glycogen storage, reduced glycogenolytic enzymes, promote blood sugar Elevated hormone deficiency, increased insulin and C-peptide or other hypoglycemic substances, tissue consumption of excessive blood sugar, and some poisoning factors such as salicylic acid and mushroom poisoning can induce hypoglycemia syndrome.

Hypoglycemia is not the essence of disease diagnosis. It is a sign of disorder of glucose metabolism. If the blood glucose level is lower than the normal range, it can be diagnosed as hypoglycemia, but the diagnosis of the cause is more difficult and complicated. The hypoglycemia is divided into:

1, fasting (fasting) hypoglycemia

(1) Endocrine and metabolic hypoglycemia:

1 insulin or insulin-like factor excess:

Increased secretion of organic insulin.

A. insulinoma, adenoma, microadenomas, carcinoma, ectopic insulinoma; B. islet B cell proliferation; islet cell diffuse hyperplasia; C. multiple endocrine neoplasia type I with insulinoma; D. pancreatic duct Cell neonatal islets.

Relative insulin increase: A. reduction of glucagon secretion by islet A cells; B. advanced stage of diabetic nephropathy and/or non-diabetic renal insufficiency; C. neonates born of diabetes; D. hyperactivity and/or The food intake has plummeted.

Non-islet B cell neoplastic hypoglycemia: A. Cancerous hypoglycemia, such as: lung cancer, gastric cancer, breast cancer, pancreatic cancer, hepatocellular carcinoma, cholangiocarcinoma, cecal cancer, colon cancer, adrenocortical carcinoma, carcinoid, etc. B. neoplastic hypoglycemia, such as: stromal cell tumor, leiomyosarcoma, neurofibromatosis, reticulum sarcoma, spindle cell fibrosarcoma, liposarcoma, rhabdomyosarcoma, stromal tumor, pheochromocytoma, nerve Maternal tumors, high-grade ganglion tumors, etc.

2 anti-insulin hormone deficiency: common pituitary dysfunction, pituitary tumor surgery, pituitary tumor after radiotherapy or corpuscular injury; single ACTH or growth hormone deficiency; hypothyroidism or mucinous edema; primary or secondary, acute Or chronic adrenal insufficiency; multiple glandular dysfunction.

(2) Insufficient intake of sugar:

1 The intake is too low, absorbing synthetic barriers.

2 long-term hunger or over-controlled diet.

3 small intestine malabsorption, long-term diarrhea.

4 excessive heat loss, such as: early pregnancy, lactation; intense activity, long-term fever; repeated dialysis.

(3) Liver disease hypoglycemia:

1 liver parenchymal cells are extensively damaged.

2 liver enzymes are disorders of glucose metabolism.

3 liver glycogen consumption is excessive.

2, after meals (reactive) hypoglycemia

(1) Type 1 diabetes early.

(2) After partial gastrectomy, it is also called hypoglycemia after a meal.

(3) Gastrointestinal dysfunction syndrome.

(4) Children, infants with idiopathic hypoglycemia (including congenital metabolic disorders).

(5) Idiopathic (ie, unexplained) functional hypoglycemia and autoimmune hypoglycemia.

3, drugs (inducible) hypoglycemia

(1) hypoglycemic agents induced hypoglycemia:

1 insulin is too large or relatively large or unstable diabetes; 2 sulfonylurea hypoglycemic agents, especially glibenclamide (glibenclamide) are more common; 3 biguanide and -glucosidase inhibitors lower blood sugar The drug is less common.

(2) Non-hypoglycemic drugs-induced hypoglycemia: common with salicylates, antihistamines, phenylbutazone, acetaminophen, tetracyclines, isoniazid, phentolamine, lishepine, Methimazole, methyldopa, monoamine oxidase inhibitors, alcoholic hypoglycemia, etc., about 50 drugs can induce hypoglycemia.

4. Asymptomatic hypoglycemia

Second, the pathogenesis

Hypoglycemia is mainly responsible for damage to the nerves. Brain and sympathetic nerves are the most important. In 1971, Briely found that hypoglycemia brain lesions are similar to ischemic cytopathic lesions. The basic lesions are neuronal degeneration, necrosis and glial infiltration, and brain metabolism. Energy mainly depends on glucose. The nerve cells have limited glycogen storage and are supplied by blood sugar. The nervous system is insensitive to hypoglycemia. The cerebral cortex, hippocampus, cerebellum, caudate nucleus and globus pallidus are most sensitive, and the thalamus is lower. The thalamus, brainstem, and cerebral nucleus are the second, and finally the anterior horn cells and peripheral nerves at the level of the spinal cord. Histological changes are the chromatin condensation and dissolution of the nerve cell nucleus, the nuclear membrane is unclear, the cytoplasm is swollen, and the small vacuoles are contained. And granules, in 1973, Chang injected mice with 2 units of human insulin, 15 to 20 minutes after the mice became lethargic, 30 to 75 minutes of mice myoclonus, seizures, 40 to 120 minutes into the coma, blood glucose in the sleepy mice The 6.72 mmol/L (120 mg/dl) was reduced to 1.18 mmol/L (21 mg/dl), and the blood glucose level in the comatose mice was only 1.01 mmoL/L (18 mg/dl).

Sugar, fat and amino acids are the sources of energy in neuro-metabolism. These substances are oxidized and released for energy storage in ATP and creatine phosphate. When needed, they are released when needed. When sugar and oxygen are reduced, ATP phosphate creatine, ganglioside Combined with reduced glucose synthesis, due to less ATP, and decreased nucleotide synthesis, resulting in neurological dysfunction, the metabolism and neurological function of high-energy phosphate complexes in hypoglycemia are not only related to blood glucose levels, but also related to oxygen partial pressure. Close, hypoglycemia due to decreased cerebral oxygen uptake, glucose uptake rate is also inhibited, relying solely on sugar to maintain oxidative metabolism levels, will inevitably affect the metabolism of fatty acids and amino acids, brain phospholipids can be reduced by 35%, brain tissue is low When blood sugar is present, the cerebral cortex is first inhibited, and then the subcortical center is involved, affecting the midbrain. Finally, the brain is damaged and a series of clinical abnormalities occur. When the blood sugar is lowered, the body has a self-regulating mechanism that stimulates adrenaline secretion and promotes Hepatic glycogen decomposes, causing blood sugar to rise to normal levels.

Establishing a related anti-regulatory mechanism of glucose (also known as counter-regulatory hormone) is to prevent the blood sugar from significantly reducing the protective mechanism of brain function. Glucose against regulating damage means that the plasma glucose concentration cannot be maintained at a normal level or can not prevent further decline of blood glucose. status.

1. Hypoglycemia has been widely concerned with the secretion of anti-regulatory hormones. The role of experimentally induced attenuation of insulin is an important factor in restoring blood sugar levels, inhibiting the release of hepatic glycogen and increasing the utilization of glucose induced by peripheral insulin, resulting in low The triggering factor of blood sugar reverses the decline of some plasma insulin. It is the key to avoid the blood sugar level of hypoglycemia in diabetic patients treated with insulin. The secretion of anti-regulatory hormone can outperform the effect of insulin, even when the plasma insulin concentration does not decrease. The same is true, in the anti-regulatory hormones, such as adrenaline, glucocorticoids, glucagon, growth hormone, etc. have obvious anti-insulin effect, these hormones are secreted immediately when plasma glucose drops to the threshold, rapidly induce hepatic glucose Heterologous, the respective effects of these hormones are similar to hepatic glucose production. Therefore, the response of any hormone is insufficient, and glucose can not completely damage the regulation function. In clinically, type 1 diabetes patients have hypoglycemia and glucagon secretion. Significantly reduced, appropriate after adrenalectomy Glucocorticoid replacement is also normal in patients with alpha, beta adrenergic blockers. Glucose resistance regulation is normal. After several years of special type of diabetes, there are some reasons for glucagon and adrenaline. Insufficient hormones cause a tendency for these patients to have severe or prolonged hypoglycemia.

2. Anti-regulatory hormones not only have an effect on the recovery of blood sugar, but also are important for maintaining the stability of glucose in the late stage. However, in the maintenance of high glucose, the sustained output of hepatic glucose, steroid hormones and growth hormone have a significant effect, and recovery in hypoglycemia. During the period, these hormones and adrenaline can reduce the utilization of peripheral glucose. The effect may be direct or indirect (such as FFA is stimulated release). In patients with insulin-dependent diabetes, the glucose uptake is reduced due to hepatic glucose release. The key to hypoglycemia recovery, long-term pituitary hypofunction, growth hormone and glucocorticoids and other anti-hormone deficiency are also important causes of severe hypoglycemia.

3, hormones against hypoglycemia, anti-regulatory function damage is common, some patients with islet cell tumors, anti-regulatory hormone secretion is reduced, but this phenomenon can be reversed after surgery, clinical glucose resistance regulation is characterized by undetected hypoglycemia Symptoms, which are the result of an adrenal reaction injury to the disease, which can lead to severe prolonged hypoglycemia.

4. The normal blood sugar level in the fasting state depends on the following three factors:

(1) The basic hormone level environment, such as glucagon, growth hormone and steroid hormone secretion and insulin secretion decreased;

(2) complete glycogenolysis and gluconeogenesis;

(3) Increased hepatic glucose production and decreased use of glucose around, but severe defense damage will lead to severe prolongation of hypoglycemia.

Low blood sugar prevention

Hypoglycemia is common in clinical practice, and hypoglycemia can be prevented. The episode of hypoglycemia can cause physical and mental health, especially to the central nervous system, and even death. Therefore, active prevention is particularly important because of the variety of causes of hypoglycemia. Sexuality and complexity, and thus preventive measures vary widely.

1, clinically more common with drug-induced hypoglycemia

Diabetes patients with insulin, sulfonylurea drugs, especially for patients with liver and renal insufficiency, insulin, sulfonylurea drugs should be gradually increased during the treatment, avoid excessive addition, insulin injection or oral hypoglycemic Eating on time, should also avoid excessive exercise intensity, and closely monitor blood sugar, especially in the intensive insulin treatment period, diabetic patients and their families should be familiar with this reaction, early prevention, early detection and early treatment, pay attention to the Somogyi phenomenon, so as not to occur Insulin dose adjustment error.

2, the use of hypoglycemic agents for the elderly should be cautious

Long-acting sulfonylureas, especially glibenclamide, should be used with caution. The early symptoms of hypoglycemia are not obvious. When the symptoms are serious, the glucose should be infused immediately, at least for 72 hours. Continuously monitor blood glucose levels and adjust treatments in a timely manner.

3, the use of sulfonylurea drugs may interact with other drugs, such as salicylic acid preparations, sulfa drugs, phenylbutazone, chloramphenicol, sputum, and blood equality, can reduce gluconeogenesis, Reduce the binding of sulfonylurea to plasma proteins, reduce the metabolism of drugs in the liver and renal excretion, and enhance the hypoglycemic effect of sulfonylureas. Therefore, attention should be paid to the use of enhanced sulfonylureas to avoid hypoglycemia. disease.

4, suspected B cell tumors, should be tested as soon as possible after starvation experiments and exercise experiments, determination of plasma insulin-C peptide concentration, and B-ultrasound, CT and other imaging examinations, for early detection, early diagnosis, early surgical treatment, Prevent the onset of hypoglycemia.

5, for patients with idiopathic functional hypoglycemia, explain the nature of the disease, give psychoanalysis and comfort work, encourage patients to exercise, diet structure to improve protein, fat content, reduce sugar, small meals, enter Dry food, avoid hunger, in addition, add fiber (non-absorbent carbohydrates if glue) to the food can help, you can also try a small dose of anti-anxiety stabilizer such as diazepam.

6, because ethanol can block hepatic gluconeogenesis and promote insulin secretion, often occurs after eating too little and 8~12h after excessive drinking, so avoid heavy drinking, especially those who eat less, due to the intake of fructose, galactose or Leucine-induced hypoglycemia is prevented by limiting or preventing the ingestion of these substances.

7. For most of the stomach resection, gastric-jejunum anastomosis, pyloric angioplasty with or without vagus nerve resection, food quickly enters the small intestine after eating, resulting in rapid absorption of food, promoting premature insulin secretion, causing hypoglycemia Therefore, it should be avoided to enter the fluid and eat fast, should be repeated several times, a small amount of high protein, low carbohydrate diet.

8, Addison disease, hypopituitarism, hypothyroidism, hypothyroidism is particularly sensitive to insulin, oral hypoglycemic agents, easy to cause hypoglycemia, should pay special attention.

Hypoglycemia Complications cerebral edema dementia coma shock

If hypoglycemia can not be alleviated, the blood glucose concentration will continue to decrease for more than 6 hours, which may cause irreversible morphological changes in brain cells, such as congestion, multiple punctiform hemorrhage, and damage to brain tissue. If correct diagnosis and treatment cannot be made in time, Brain edema, ischemic punctate necrosis, brain softening, dementia, coma, shock and even death. Hypoglycemia is not an independent disease. Many causes can cause hypoglycemia. The cause of hypoglycemia should also be checked after diagnosis.

Symptoms of hypoglycemia Common symptoms Neurotic personality Hypoglycemia Convulsion vertigo Tremors weakness Wood stiffness Heart vision Discomfort Anxiety anxiety

1. According to the cause, the classification is as follows

(1) islet hyperfunction: islet B cell proliferation, adenoma and carcinoma, such as islet cell tumor, functional B cell secretion defects, latent diabetes, familial multiple endocrine neoplasia (including insulinoma, pituitary tumor and Parathyroid adenoma, etc.).

Symptoms that stimulate sympathetic stimulation of the adrenal gland include anxiety, tremors, palpitations, and hunger. These symptoms are often warning signs of hypoglycemia, leading to hemodynamic changes including tachycardia, increased pulse pressure, and changes in the ECG, such as the ST segment. Downward movement, T wave low level and QT interval prolongation and arrhythmia, especially ectopic atrial or ventricular arrhythmia, severe cases can cause angina pectoris or myocardial infarction and aggravation of retinopathy and other complications, or serious Patients with dullness can show hypothermia, which is particularly pronounced in alcohol-induced hypoglycemia. Like many other signs, peripheral circulatory failure can occur, leading to shock and death.

(2) other endocrine gland diseases: such as hypothyroidism, adrenal insufficiency, hypopituitarism (including growth hormone deficiency, adrenocortical hormone deficiency, thyroid stimulating hormone deficiency), pancreatic islet cell damage caused by glucagon Lack of waiting.

(3) Liver disease: such as severe hepatitis, cirrhosis, liver cancer, liver necrosis and Reye syndrome (fatty liver, encephalopathy, hypoglycemia syndrome).

(4) hereditary liver enzyme deficiency: such as glycogen accumulation disease, galactosemia and fructose intolerance.

(5) Digestive diseases: such as gastrointestinal surgery, peptic ulcer disease, acute gastroenteritis, chronic gastroenteritis, duodenitis, digestive system tumors, chronic diarrhea and malabsorption and excessive consumption.

(6) Drug-induced: such as insulin, glibenclamide in sulfonylureas, phenformin in bismuth hypoglycemic agents, etc., others such as ethanol, sodium salicylate, phentolamine, isoniazid, phenylbutazone, antihistamine preparation, monoamine oxidase inhibitor, propranolol (40mg or more per day), aspirin combined with D860 can cause hypoglycemia.

(7) severe malnutrition: such as intestinal malabsorption syndrome, Crohn's disease, chronic enteritis, hunger malnutrition and fasting can cause hypoglycemia.

(8) Central nervous system diseases: such as birth injury, developmental disorders and retardation, brain jaundice, traffic hydrocephalus, hypothalamic and brain stem lesions, brain hypoplasia, etc. can cause hypoglycemia.

(9) transient neonatal: such as premature infants, infants with diabetic mothers have transient islet hyperfunction, transient erythrocytosis in erythrocyte hyperplasia infants, Rh factor immune factors make a large number of red blood cells hemolyzed, after birth Hypoglycemia can occur in 2 to 3 days. Under the action of maternal hyperglycemia, B cells proliferate and insulin secretion increases. Failure to correct in time may result in transient hypoglycemia.

Multiple changes in the clinical manifestations of hypoglycemia may complicate the diagnosis: these symptoms can recur in the onset of hypoglycemia, even for a few minutes to a few hours. This relatively short duration is due to endogenous glycemic confrontation. Regulatory mechanisms and intake of sugars restore blood glucose levels to normal. Without these adjustments, blood glucose levels continue to decrease and can even cause loss of consciousness, the severity of epilepsy or coma, if the patient complains of long-term fatigue, burnout or hours or I can't concentrate for a few days. These reasons are not only due to hypoglycemia.

When the symptoms are relieved after ingesting carbohydrates, not only due to hidden hypoglycemia, the corresponding symptom relief of glucose intake is not a specific manifestation of hypoglycemia. Many anxiety-related symptoms can be confirmed by eating. Hypoglycemia.

(10) extra-pancreatic neoplasia: generally believed to be caused by ectopic insulin or due to insulin-like active substances including some insulin-like activity factors, more common in thoracic and abdominal cavity tumors, such as fibrosarcoma, mesothelioma, abdominal mucus Tumor, cholangiocarcinoma, adrenocortical carcinoma, renal blastoma, lymphoma, gastrointestinal cancer, lung cancer and liver cancer and ovarian cancer, etc., generally larger, weighing up to 500-1000 grams, can secrete insulin-like growth factor Wait.

(11) Renal glucosuria: When the urine sugar is lost too much, the blood sugar level drops, and the incidence rate is 1% of diabetes, which is a family hereditary disease caused by a low renal sugar threshold.

(12) Infectious disease: Phillips report (1989) falciparum malaria can be associated with hypoglycemia.

(13) bacterial sepsis septic: sepsis, sepsis, pneumonia and cellulitis can be associated with hypoglycemia.

(14) Others: such as ketosis hypoglycemia, leucine-sensitive hypoglycemia, familial hypoglycemia, poisoning factors (mushroom poisoning, sputum fruit poisoning, etc.), long-term fever, lactation and pregnancy, chronic diseases and unknown causes Factors such as hypoglycemia can occur.

2, the symptoms and signs of hypoglycemia can have the following clinical manifestations

(1) Sympathetic nervous system excitatory performance: After the occurrence of hypoglycemia, the secretion of adrenaline is increased, and hypoglycemia syndrome may occur. This is a compensatory response to hypoglycemia. The patient has pale complexion, palpitations, cold limbs, cold sweat, and hand tremor. The legs are soft, the body is weak, dizziness, vertigo, hunger, panic and anxiety, etc., relieve after eating.

(2) Symptoms of disturbance of consciousness: inhibition of cerebral cortex, consciousness, orientation, loss of recognition, lethargy, sweating, tremor, memory impairment, headache, apathy, depression, dream state, severe dementia, some people There are strange behaviors, etc. These neuropsychiatric symptoms are often mistaken for mental disorders.

(3) Epilepsy symptoms: When hypoglycemia develops to the midbrain, muscle tension is enhanced, paroxysmal convulsions, seizures or epileptic seizures occur, and the seizures are mostly episodes, or status epilepticus, when the brain is affected, the patient Can enter the coma, go to the state of the brain stiff, bradycardia, body temperature does not rise, all kinds of reflexes disappear.

(4) Symptoms of pyramidal and extrapyramidal involvement: When the subcortical center is inhibited, the mind is unclear, restless, hypersensitivity, allergic dance movements, dilated pupils, and even tonic convulsions, extrapyramidal Cone beam sign positive, can be characterized by hemiplegia, palsy, aphasia and monoterpene, etc. These performances are mostly temporary damage, which can be quickly improved after glucose. Extrapyramidal damage can affect globus pallidus, caudate nucleus, shell The brain tissue structure of the nucleus and the cerebellar dentate nucleus is often characterized by tremor, euphoria and hyperkinesia, and torsion.

(5) Cerebellar involvement: hypoglycemia can damage the cerebellum, manifested by ataxia, uncoordinated movement, inaccurate distance, low muscle tone and abnormal gait, especially in the late stage of hypoglycemia, often with ataxia and dementia .

(6) manifestations of cranial nerve damage: hypoglycemia may have cranial nerve damage, manifested as vision and visual field abnormalities, diplopia, dizziness, facial nerve paralysis, difficulty swallowing and hoarseness.

(7) Peripheral nerve damage: late hyperglycemia often occurs peripheral neuropathy and causes muscle atrophy and paresthesia, such as limb numbness, muscle weakness or muscle twitch, etc. Clinically, patients with hypoglycemia have a gloved sleeve at the distal end of the limb. Patients with abnormalities may also have peripheral stimuli and burning changes, which are related to cell degeneration of the anterior horn of the spinal cord. Others believe that hypoglycemia caused by hypoglycemia caused by insulinoma is related to myositis. Hypoglycemic peripheral nerve The lesion can also cause the foot to sag, the hand and foot fine movement failure, such as can not write, can not eat, can not walk, or even bedridden.

(8) hypoglycemia caused by organic lesions: the most common in insulinoma hypoglycemia, about 70% of benign adenomas, diameter 0.5 ~ 3.0cm, mostly located in the tail of the pancreas, the onset of the pancreas and pancreatic head The situation is similar, mostly single, hyperplasia, cancer is rare, such as cancer and more liver and adjacent tissue metastasis, domestic Hu Lixin has reported a case of multiple insulinoma, a total of 7, pancreatic head 1, pancreas Body 2, pancreatic tail 4, different size, diameter 10 ~ 50mm, the smallest reported 1mm, called micro adenoma, difficult to be found during surgery.

Insulinoma has a heavier and longer-lasting episode of hypoglycemia, and often has the following characteristics: 1 more hypoglycemia occurs on an empty stomach, such as before breakfast; 2 symptoms are mild and heavy at the time of onset, from fewer to more, gradually more frequent; 3 symptoms For paroxysmal attacks, the situation at the time of the attack, the patients themselves often can not recall; 4 different patients with hypoglycemia symptoms are not exactly the same, the same patient sometimes does not have the same symptoms every time; 5 hypoglycemia patients often can not tolerate hunger, It is often increased before eating to prevent seizures, so the patient's weight generally increases; 6 patients with fasting blood glucose can be very low, sometimes only 0.56 ~ 1.68mmol / L (10 ~ 30mg / dl).

(9) Reactive functional hypoglycemia: Reactive functional hypoglycemia Main manifestations: 1 more common in women, less episodes, longer history, more emotional tension and traumatic history; 2 hypoglycemia episodes after meals 2 ~3h, fasting blood glucose is normal or slightly lower; 3 low blood sugar episodes are mainly adrenaline-induced symptoms, lasting 20 ~ 30min, often no coma, more self-relieving; 4 patients are often neurotic, fat, negative signs, although repeated attacks The condition did not deteriorate; 5 low blood sugar level was not as obvious as insulinoma, fasting blood glucose was 2.24 ~ 3.36mmol / L (40 ~ 60mg / dl); 6 patients can tolerate hunger for 72h long without coma.

Generally, the blood cells in the brain receive a relatively constant glucose from the bloodstream, which is not affected by the growth and decline of blood glucose. Therefore, the symptoms of hypoglycemia should be expressed below 45 mg/dl (2.52 mmol/L). The hypoglycemia is similar to the hypoxia state of the brain. Therefore, when there are cerebral circulation disorders (such as arteriosclerosis, cerebral infarction), symptoms of hypoglycemia may appear in advance, and the degree and speed of blood glucose reduction are roughly parallel to the appearance and severity of clinical symptoms, but there is no absolute quantitative relationship, and symptoms of hypoglycemia occur. The blood glucose threshold has no uniform standard, and the individual difference is large. The same blood glucose value is 30mg/dl (1.68mmol/L). Some of them have coma, some have only some symptoms of hypoglycemia and no coma, but they all need treatment. Improve blood sugar levels.

Hypoglycemia check

Laboratory inspection:

1, fasting plasma insulin and blood glucose determination

Non-obese people with fasting insulin levels higher than 24U/ml can be considered hyperinsulinemia. However, even if the fasting insulin value is normal, the relative blood glucose level has increased. When the fasting blood glucose is lower than 2.8mmol/L, plasma insulin should be reduced to 10U/ Below ml, the plasma glucose level is lower than 2.2mmol/L, the insulin value will be lower than 5U/ml, and the insulin to blood glucose ratio (I:G) is also generally reduced. If the I:G value is increased or >0.3, high insulin blood should be suspected. Symptoms, I: G> 0.4 suggest that insulinoma may be.

2. Oral glucose tolerance test (OGTT)

To determine whether there is fasting hypoglycemia, OGTT has no meaning. For example, the glucose tolerance test is extended to 4 to 5 hours, which is valuable for the diagnosis of postprandial hypoglycemia.

3. Determination of plasma proinsulin and C peptide

Normal plasma contains a small amount of proinsulin. Most patients with insulinoma have elevated levels of proinsulin in the blood circulation. Under normal circumstances, proinsulin generally does not exceed 22% of total immunoreactive insulin, and more than 85% of insulinoma patients have insulin. The percentage is over 25%.

The plasma insulin value measured by the RIA method is called immunoreactive insulin. This is because the polyclonal antibody of insulin cross-reacts with insulin analogs such as proinsulin, and the normal value of insulin is low, so the result is very careful.

C-peptide determination can be used for the identification of endogenous and exogenous hyperinsulinemia. C-peptide and insulin are secreted by equal molecular weight. Blood C-peptide is not detected in exogenous hyperinsulinemia. C-peptide level High suggestive of endogenous hyperinsulinemia, conversely, low C-peptide levels suggest that elevated plasma insulin levels are caused by exogenous insulin.

4, insulin antibody, insulin receptor antibody determination

The presence of insulin antibodies in plasma suggests that insulin or autoimmune insulin syndrome has been used in the past. The autoantibodies of insulin can be classified into endogenous and exogenous depending on the source of the antigen. The biological activity and effect of the antibody are excitatory. Divided into inhibitory autoantibodies.

Patients who have been treated with insulin for a long time can produce anti-insulin antibodies, which are related to the structure of insulin and human insulin in the preparation and the impure preparation, but the use of unimodal human insulin or recombinant human insulin can still produce insulin antibodies, such antibodies It is one of the important reasons for insulin insensitivity.

Some diabetic patients who have never used insulin can produce anti-insulin autoantibodies, which are characterized by a low concentration of free insulin and a marked increase in the total amount of insulin. This insulin resistance syndrome patient often needs a large dose of insulin to control. High blood sugar status.

Another rare case is that the body's own anti-insulin antibodies can excite the insulin receptor and cause severe hypoglycemia, as described later.

5. Determination of plasma sulfonylurea drugs and their metabolites in urine

Determination of plasma sulfonylurea drugs or their urinary metabolites can help determine the diagnosis of hyperinsulinemia induced by sulfonylurea drugs. Chloramphenazone has a long half-life and is associated with a higher risk of hypoglycemia.

6, insulin inhibition test

Asymptomatic fasting hypoglycemia or instability or marginal hyperinsulinemia, inhibition tests can be used to identify whether endogenous insulin secretion is excessive.

Exogenous insulin can not completely inhibit the release of insulinoma C-peptide and proinsulin. However, it has been reported that the C-peptide inhibition test of some patients with insulinoma can be normal. Kim et al found that after applying exogenous insulin in normal people, Plasma C-peptide inhibits about 66%, but in patients with insulinoma, plasma insulin and C-peptide are not inhibited when blood glucose is normal, and endogenous insulin and C-peptide are inhibited during hypoglycemia.

7. Stimulation test

The sensitivity of the suspicious fasting hypoglycemia stimulation test is lower than the I:G ratio, C peptide, proinsulin determination, etc. The commonly used stimulation tests include tolbutamide, arginine and glucagon stimulation test, 80 % of insulinoma patients with abnormal tolbutamide test, 74% had abnormal arginine test, 58% had abnormal glucagon test, and calcium injection stimulated insulin secretion in insulinoma patients, but it was also reported that insulin Insulin secretion does not increase after injection of calcium in patients with tumors.

8. Diagnosis of congenital metabolic diseases with hypoglycemia

There are many diagnostic methods, which can be selected according to needs. The diagnosis depends on the pathological diagnosis and genetic analysis of enzyme defects.

(1) Glycemic index: The glycemic index refers to the relative ability of carbohydrates to raise blood sugar. Compared with carbohydrates with low glycemic index, higher glycemic index carbohydrates can raise blood sugar to a higher level and are faster. According to different glycemic index, carbohydrates can generally be divided into several types. Amylose reacts slowly and weakly to blood sugar and blood insulin, while amylopectin can significantly increase blood sugar, insulin and glucagon.

(2) Fructose tolerance test: After oral administration of fructose 200mg/kg, the response of normal people is similar to that of OGTT, while hereditary fructose intolerance is hypoglycemia due to deficiency of fructose-1-phosphate aldolase, hypophosphatemia And fruit diabetes.

(3) Glucagon test: Glucagon only acts on liver phosphorylase, which has no effect on muscle phosphorylase. After normal humans inject 1 mg of glucagon in fasting muscle, blood glucose rises, and the peak is seen in 45 minutes. Left and right, blood insulin and blood sugar levels are consistent, insulinoma blood sugar peaks can appear early, but decline rapidly, and hypoglycemia, blood insulin secretion is higher than normal, glycogen accumulation disease (GSD) type I no blood sugar peak or A small peak is seen after 1 hour, blood lactate is significantly elevated, blood pH and HCO3- decreased, this test can also be used for the differential diagnosis of other hypoglycemia.

(4) Adrenalin test GSDI type blood glucose increase after injection of adrenaline does not exceed 30%, because GSD may also affect the neutrophil glucose metabolism, so the use of adrenaline, blood neutrophil rise is not obvious, However, a convenient method for the diagnosis of GSDLb is to stimulate the activity of NAPDH oxidase with phoorbol-myristate-acetate to assist in the diagnosis of GSDLb and neutrophil dysfunction.

(5) Ischemic exercise lactic acid test: Wrap the upper arm around the sphygmomanometer cuff, pressurize it to 200mmHg, and let the patient grasp the activity for 1 minute, determine the blood lactate value before and after the test, and increase the blood lactate after the normal test. More than double, type III, V-type GSD does not increase, but can not rule out other causes of lactic acid formation disorders (such as muscle phosphofructokinase defects, etc.).

(6) clonidine treatment test: if it is suspected to be GSD, commonly used clonidine (0.15mg / d, or 0.2mg / M2 body surface area per day) for several months, GSD (such as I, III, VI) can be increased The body's mechanism of action is unclear, so the drug is also effective for growth retardation caused by short stature and other causes, so it may be related to its role in the central nervous system and promotion of GH secretion.

(7) Other tests: analysis of amino acid composition of blood, urine and cerebrospinal fluid contributes to the diagnosis of amino acid metabolic diseases. Blood ketone, blood sugar, blood nitrogen and creatine kinase are basic testing items for various hypoglycemia, if possible As far as possible, the enzyme activity measurement of the diseased tissue and the determination of abnormal glycogen particles, metabolic substrates, etc., and the molecular biology method to identify the mutation of the enzyme gene can confirm the type and site of the enzyme defect.

9, chromogranin A (CgA)

Chromogranin A (CgA) is one of the markers of neuroendocrine tumors. About 90% of APUD tumor patients have elevated serum CgA. In midgut-derived carcinoid patients, blood CgA can be increased by tens to several. A hundred times, after liver metastasis, the increase of blood CgA is more obvious (CgA error measured by RIA method is 30% to 40%).

10. Determination of other APUD hormones and metabolites

Corresponding peptides or amine hormones can be determined according to clinical manifestations, but they are generally difficult to spread due to their high cost. In most cases, urine 5-hydroxyindoleacetic acid (5-HIAA) and insulin in the gastric juice, proinsulin and C can be measured. Peptide, if necessary, can be used to determine gastrin. If you want to determine the growth potential of the tumor, determine the prognosis, you can determine Ki-67 protein and PCNA (proliferating cell nuclear antigen), tumor tissue can be used as adhesion molecule CD44 and platelet-derived Growth factor alpha (PDGFa) receptor staining, somatostatin receptor subtype analysis and PKR assay are also helpful for diagnosis.

Film degree exam:

1, EEG

Similar to hypoxia, there is no specific change, slow wave or other changes, long-term hypoglycemia can have abnormal changes in brain lesions.

2, EMG

The nerve conduction time is normal, the distal muscle has denervation, the number of motor unit potential is reduced, the diffuse denervation fiber, the tip and the large motor unit discharge, and the multi-phase potential are more consistent with the changes of peripheral neuron or anterior horn cell type.

3, X-ray inspection

Occasionally, calcified adenomas, adjacent organs are distorted or displaced, pancreatic angiography shows increased blood supply, selective superior mesenteric artery, and celiac angiography contribute to lesion localization.

4, CT and MRI scan

Space-occupying lesions in the abdominal cavity and pancreas can be found.

5, B-ultrasound

Tumors of the pancreas can be found, and those less than 1 cm are easily missed, which is not as reliable as CT and MRI.

6, other

Pancreatic radionuclide scanning, ECT scanning, and 75Se-methionine examination can detect space-occupying lesions inside and outside the pancreas.

Hypoglycemia diagnosis

Diagnostic criteria

The main reason for the difficulty in diagnosis is due to the onset of illness, and the clinical symptoms, signs and biochemical abnormalities are intertwined, so it is easy to be misdiagnosed and missed clinically, but mainly depends on the blood sugar level. All healthy people including women and children, when the fasting vein When the plasma glucose value is lower than 2.8mmol/L (50g/dl), although there is no clinical symptoms, the signs should be diagnosed as hypoglycemia, and fasting venous blood glucose above 3.9mmol/L (70mg/dl) can rule out hypoglycemia. Fasting venous plasma glucose 2.8 ~ 3.9mmol / L (50 ~ 70mg / dl) may suggest hypoglycemia, but very few healthy women after 72 hours of fasting blood sugar as low as 1.4 ~ 1.7mmol / L (25 ~ 30mg / Dl), even intracellular glucose levels close to 0 and neonatal blood glucose as low as 1.7mmol/L (30mg/dl) were considered normal, and some experts believe that children and infants have blood glucose levels below 2.8mmol/L (50mg). /dl), should be carefully observed, only blood glucose levels below 2.2mmol / L (40mg / dl), can be diagnosed and treated, otherwise, the elderly venous plasma glucose value is 3.3mmol / L (60mg / dl) often Hypoglycemia can occur, so normal people's blood sugar is maintained at a desirable level, 24 hours The fluctuation range rarely exceeds 2.2-2.8mmol/L (40-50mg/dl). The internal environment stability of this glucose is regulated by various hormones. Many organs, especially liver and muscle tissues, are involved in glucose metabolism, when glucose When using, ingesting and/or generating imbalance, hyperglycemia or hypoglycemia may occur. The severity and signs of clinical symptoms of hypoglycemia are not consistent with the total blood glucose level. Therefore, as an experimental diagnostic reference value, care must be taken. The following points:

1. At the same time, the arterial blood glucose level is usually slightly higher than the capillary value, while the latter is higher than the intravenous value. The fasting capillary blood glucose value (measured blood glucose is whole blood) is higher than the venous blood glucose value 5% to 10%.

2, blood glucose measurement is divided into serum, whole blood, plasma three methods, determination of serum blood sugar, must be collected immediately after blood collection of serum, otherwise the time is too long, sugar decomposition, the result is low; whole blood sugar is susceptible to hematocrit and non-sugar The effect of the substance is also slightly lower than the plasma blood sugar by 5% to 10%. Therefore, in the clinic, blood glucose is measured in the clinic to judge various causes of hyperglycemia and hypoglycemia.

3, for unknown reasons, persistent or recurrent hypoglycemia, should always monitor blood insulin, C-peptide, proinsulin and blood, sulfonylurea concentration, to identify, such as hyperinsulinemia can be found in insulinoma, sulphur Urea drugs, autoimmune hypoglycemia and topical insulin; and elevated blood C peptide only found in insulinomas and sulfonylureas.

Differential diagnosis

1. For episodes (especially on fasting), psycho-neural abnormalities, convulsions, abnormal behavior, disturbance of consciousness or coma, especially for diabetic patients treated with insulin or oral hypoglycemic agents, should consider the possibility of hypoglycemia. Timely check blood sugar, it is worth noting that some patients with hypoglycemia have normal blood sugar at the time of treatment, and there is no symptoms of hypoglycemia, often only manifested as sequelae of chronic hypoglycemia, such as hemiplegia, dementia, epilepsy, mental disorders, children's IQ is significantly lower, etc. As a result, clinical diagnosis is often misdiagnosed as mental illness, epilepsy or other organic encephalopathy (such as encephalitis). Therefore, it should be differentiated from other diseases of the central nervous system organic disease, such as encephalitis, multiple sclerosis, cerebrovascular accident. , epilepsy, diabetic ketoacidosis coma, diabetes non-ketotic hyperosmolar coma, psychosis, drug poisoning, etc.

2, fasting, a few hours after a meal or after physical activity, sympathetic excitation is the main manifestation of hypoglycemia, should be associated with sympathetic excitation, such as hyperthyroidism, pheochromocytoma, autonomic dysfunction, Diagnostic differentiation of diabetic autonomic neuropathy, menopausal syndrome, etc.

3, hypoglycemia after alcoholism should be distinguished from alcoholism. Ethanol can not only cause hypoglycemia, but also cause ketosis. Sometimes hypoglycemia and ketosis caused by ethanol can be mistaken for diabetic ketoacidosis. This is a diagnosis. Need to pay attention to.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.