hypoglycemia syndrome
Introduction
Introduction to hypoglycemia syndrome 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. The disease is often misdiagnosed as rickets, epilepsy, mental illness, brain tumors and encephalitis. 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 The neuropathy is irreversible and the consequences are poor. basic knowledge Sickness ratio: 2% Susceptible people: no specific people Mode of infection: non-infectious Complications: pancreatic fistula pancreatic cyst diabetes
Cause
Causes of hypoglycemia syndrome
Causes:
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.
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 gave mice 2N of normal insulin, 15-20 min mice drowsiness, 30-75 min mice myoclonus, seizures, 40-120 min into coma, sleepy mice blood glucose from 6.72 The 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.
Prevention
Hypoglycemia syndrome prevention
prevention:
(1) Rational use of insulin. Insulin is divided into long-acting, medium-efficiency and short-acting according to the duration of its action. The insulin dose is best to ask the doctor to help adjust the condition according to the condition and food intake. In addition to the dose, pay attention to the action time. When using normal insulin, it should be taken 15 minutes before eating, but it should not exceed 30 minutes before eating, otherwise hypoglycemia may occur. If you use intermediate or long-acting insulin, you should ask your doctor to pay attention to the strongest time of insulin. It should not be placed on an empty stomach at night, otherwise nighttime hypoglycemia may occur. If you use short-acting and medium-long-acting insulin, you should pay attention to the strongest action time of the overlapping effect of the two, not on the fasting or at night, so as not to cause hypoglycemia, pay attention to clearing the highest blood sugar, and can not rule out hypoglycemia at night.
(2) Patients who inject mixed insulin should pay special attention to eating dinner on time and adding a small amount of food before going to bed at night to prevent hypoglycemia at night. Patients who are prone to hypoglycemia in the second half of the night and in the early morning should eat more staple foods such as staple foods or eggs, dried tofu, etc., which absorb slow protein.
(3) Make a good observation record of the disease, urine sugar is negative for several days, consider reducing the amount of insulin as appropriate, and add food in time before the strongest action of insulin and when there is a lot of activity.
(4) When the amount of labor increases or activities are particularly high, it is necessary to reduce the amount of insulin or add food in time. Patients who take oral hypoglycemic drugs should also reduce their dosage or make meals in time.
(5) Regular attention to diet, should be in line with the role of insulin, pay special attention to observe changes in urine sugar, before the most powerful moment of insulin, timely meals.
(6) All diabetics should always carry some fruit sugar and biscuits with them to correct hypoglycemia at any time.
Complication
Hypoglycemia syndrome complications Complications pancreatic fistula pancreatic diabetes
In the case of insulin hyperplasia, postoperative complications include pancreatic fistula, followed by pseudo pancreatic cysts, diabetes, and acute pancreatitis.
Symptom
Symptoms of hypoglycemia syndrome Common symptoms Pale pale tension Diplopia after a meal syndrome coma Heatstroke High fever Cold sweat Anxiety Hypoglycemia
General symptoms and signs:
1. Sympathetic nervous system excitatory performance Hypoglycemia stimulates the increase of adrenaline secretion, hypoglycemia syndrome can occur, which is a compensatory response to hypoglycemia, patients have pale, palpitations, cold limbs, cold sweat, hand tremors, soft legs , weakness, dizziness, vertigo, hunger, panic and anxiety, etc., relieve after eating, such as the development of hypoglycemia can appear the following clinical manifestations.
2. Symptoms of consciousness disorder Cerebral cortex is suppressed, consciousness, orientation, loss of recognition, lethargy, sweating, tremor, memory impairment, headache, apathy, depression, dream state, severe dementia, some people may be strange Behavior, 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 most of the episodes are episodes of epileptic seizures or epilepsy. When the brain is affected, the patient can enter. Coma, go to the state of the brain stiff, bradycardia, body temperature does not rise, all kinds of reflexes disappear.
4. When the pyramidal and extrapyramidal symptoms are inhibited, the subcortical center is inhibited, unclear, restless, hyperalgesia, clonic dance, dilated pupils, even tonic convulsions, extrapyramids and cones Positive signs of bundles can be characterized by hemiplegia, palsy, aphasia and monoterpene. These manifestations are mostly temporary damage, which can be quickly improved after glucose. Extrapyramidal damage can affect globus pallidus, caudate nucleus, putamen and Brain tissue structures such as the cerebellar dentate nucleus are often characterized by tremors, euphoria and hyperkinesia, and torsion.
5. Cerebellar involvement performance Hypoglycemia can damage the cerebellum, manifested as ataxia, uncoordinated movement, inaccurate distance, low muscle tone and abnormal gait, especially in the late stage of hypoglycemia, often with ataxia and dementia.
6. Cranial nerve damage performance 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 manifestations In the late stage of hypoglycemia, peripheral neuropathy often causes muscle atrophy and paresthesia, such as limb numbness, muscle weakness or muscle twitch, etc. Clinically, patients with hypoglycemia have a glove-like sensation abnormality at the distal end of the limb. There may also be 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 insulinoma is related to myositis and myositis. Hypoglycemic peripheral neuropathy Can cause foot drop, 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 is most common in insulinoma hypoglycemia, about 70% is benign adenoma, diameter 0.5 ~ 3.0cm, mostly located in the tail of the pancreas, the incidence of pancreatic body and pancreatic head is similar Most of them are single-shot, followed by hyperplasia. Carcinoma is rare. If there is more liver and adjacent tissue metastasis for cancer, Hu Lixin has reported a case of multiple insulinoma, 7 in total, pancreatic head 1, pancreatic body 2 The tail of the pancreas 4 is different in size and has a diameter of 10 to 50 mm. The smallest one is reported as 1 mm, which is called micro adenoma, which is not easy to be found during surgery.
Insulinoma has a heavier and longer-lasting episode of hypoglycemia and often has the following characteristics:
More than 1 hypoglycemia occurs on an empty stomach, such as before breakfast;
2 When the attack occurs, the symptoms are light and heavy, from small to many, and gradually become frequent;
3 symptoms are paroxysmal attacks, the situation at the time of the attack, the patient himself often can not recall;
4 The symptoms of hypoglycemia in different patients are not exactly the same, and the symptoms of each episode of the same patient are sometimes not exactly the same;
5 patients with hypoglycemia often can not tolerate hunger, often increase the intake before the onset 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 performance Reactive functional hypoglycemia main performance:
1 More common in women, less episodes, longer medical history, more emotional tension and traumatic history;
2 low blood sugar episodes are more than 2 to 3 hours after a meal, fasting blood glucose is normal or slightly lower;
3 The episode of hypoglycemia is mainly caused by the symptoms of adrenaline, which lasts for 20 to 30 minutes, often without coma, and more self-relieving;
4 patients are often neurotic, gain weight, negative signs, although repeated episodes and the condition has not deteriorated;
5 low blood sugar levels are not as obvious as insulinoma, fasting blood glucose is more than 2.24 ~ 3.36mmol / L (40 ~ 60mg / dl);
6 patients can tolerate hunger for 72 hours 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.
Examine
Examination of hypoglycemia syndrome
Laboratory inspection:
1. Fasting blood glucose should be tested for blood glucose multiple times, and the low blood sugar level is <3.36mmol/L (60ng/dl).
2. Glucose tolerance test Patients with hypoglycemia and insulinoma patients often showed hypoglycemia curves, occasionally normal values, and hypoglycemia occurred only at the onset.
3. Determination of serum insulin and C-peptide The serum insulin and C-peptide values were determined by radioimmunoassay. The normal value was (14±8.7) U/ml, the C-peptide value was 0.8-4.0 ng/ml, and the insulin value of insulinoma patients was increased. High, up to 160U / ml, C peptide value also increased accordingly.
4. Fasting test for 24h, blood sugar decreased, hypoglycemia symptoms, insulinoma patients can not tolerate, and a series of symptoms of hypoglycemia, should end the test as soon as possible, do not lead to coma, to prevent brain damage.
5. Tolbutamide (D860, Tolbutamide) test Infusion of D8601g after 15-20h, insulin can reach 100u / ml, 2 to 3h after this is in low blood sugar level, can cause severe hypoglycemia in patients, should stop if necessary In the trial, glucose was given, and functional hypoglycemia responded as usual. The blood glucose of patients with insulinoma decreased significantly.
6. Leucine test for the challenge test, intravenous injection of leucine 150mg, blood glucose decreased by 1.4mmol / L (25mg / dl) or more, suggesting insulinoma, oral L-leucine 200mg / kg body weight, before oral administration and after 10 , 20, 30, 40, 50, 60min, respectively, to detect blood sugar and insulin, because leucine can stimulate insulin secretion and release, taking 30 to 45 minutes, blood glucose drops to 50mg / dl (2.8mmol / L) or less positive .
7. The glucagon test is a challenge test. After 6-8 hours of eating, intramuscular glucagon 1 mg is administered intramuscularly. The normal blood glucose peaks in 45 minutes, and returns to normal in 2 hours. The blood glucose peak of hypoglycemia patients appears in advance, and is still in 2 hours. Obvious hypoglycemia level, insulinoma patients with intravenous glucagon 5 ~ 30 minutes, the peak insulin response is above 130U / ml, normal and non-obese people are not higher than 100U / ml, must be collected every 5 minutes 1 Once, it took 30 minutes to get the correct conclusion.
Film degree exam:
1. EEG is similar to hypoxia, no specific change, slow wave or other changes, long-term hypoglycemia can have abnormal changes in brain lesions.
2. Electromyography nerve conduction time is normal, distal muscles have denervation, motor unit potential number is reduced, diffuse denervation fibers, tip and giant motor unit discharge, multiphase potential, more consistent with peripheral neuron or anterior horn cells Type change.
3. X-ray examination occasionally calcified adenoma, adjacent organs are distorted or displaced, pancreatic artery angiography shows increased blood supply, selective superior mesenteric artery, celiac angiography is helpful for lesion localization.
4. CT and MRI scans can be found in the abdominal cavity and pancreatic sites of space-occupying lesions.
5. B-ultrasound can detect tumors in the pancreas, less than 1cm is easy to miss diagnosis, not as reliable as CT and MRI.
6. Other pancreatic radionuclide scanning, ECT scanning, 75Se-methionine examination can find space-occupying lesions inside and outside the pancreas.
Diagnosis
Diagnosis and diagnosis of hypoglycemia syndrome
The three diagnostic criteria for Whipple's hypoglycemia syndrome are:
1 fasting and exertion can induce hypoglycemic episodes;
2 clinical hypoglycemia symptoms can be quickly relieved by glucose;
3 The blood sugar of adults and children is usually lower than 2.24 ~ 2.80mmol / L (40 ~ 50mg / dl), the newborn is less than 1.68mmol / L (30mg / dl), idiopathic hypoglycemia often occurs in about 10 years old Children, hereditary liver enzyme deficiency, Reye syndrome hypoglycemia is also more common in childhood, insulinoma occurs in patients 13 to 57 years old, male: female incidence ratio is 5:1, such patients often do not tolerate hunger, there are Eating more habits, so there are more fat people, and the patient's previous health foundation is good, which helps differential diagnosis.
Differential diagnosis
There are many differential diagnosis of hypoglycemia syndrome, and should be noted when identifying:
1 year old body failure, mild patients, individual differences in patients with atherosclerosis;
2 with hypopituitarism, adrenal insufficiency and hypothyroidism;
3 diabetes maternal;
4 severe hepatitis, nephritis;
5 and the use of potential hypoglycemic drugs, such as phenylbutazone, sulfamethoxazole, chloramphenicol and dicoumarin, can strengthen the role of D860, stimulate insulin secretion and lower blood sugar.
According to the Whipple triad, the accuracy of diagnosis of hypoglycemia can reach 91%. Adding medical history, blood glucose and serum insulin determination can improve the diagnostic level. Generally, D860, L-leucine and glucagon test are rarely used clinically. Various tests can be selectively performed. OGTT insulin release test and fasting test are commonly used. The amount of insulin released by normal human pancreatic cells under different factors is different, and at least the order is glucose tolerance test>D860 test>pancreas Glucosamine test>leucine test, and the order of insulinoma is glucagon test>D860 test>leucine test>glucose tolerance test, low sensitivity to glucose, should be associated with epilepsy, syncope, brain Tumor, diabetic ketoacidosis coma, parathyroidism, extracerebral extravascular, uremia, snoring, hepatic coma, etc. for differential diagnosis.
