What Is Nocturnal Hypoglycemia?

Hypoglycemia syndrome

Hypoglycemia syndrome (hypoglycemicsyndrome) is a group of syndromes caused by multiple causes. The blood glucose concentration is usually lower than 3.36mmol / L (60mg / dl), and severe and long-term hypoglycemia can cause extensive neurological damage and complications. Patients have pale, palpitations, cold limbs, cold sweats, hand tremor, soft legs, fatigue, dizziness, dizziness, hunger, panic and anxiety, etc., and alleviate after eating. If hypoglycemia gradually develops, the following clinical manifestations may appear.

Detailed hypoglycemia syndrome

Common functional hypoglycemia and liver-derived hypoglycemia, followed by hypoglycemia caused by insulinoma and other endocrine diseases. The disease is often misdiagnosed as rickets, epilepsy, psychosis, brain tumors and encephalitis. After proper treatment, the symptoms can quickly improve. Early identification of this disease is very important and can achieve the purpose of cure. Delayed diagnosis and treatment will cause permanent neuropathy and cannot be reversed, with poor consequences.

Signs and manifestations of hypoglycemia syndrome

The symptoms and signs of hypoglycemia can have the following clinical manifestations.

1. Sympathetic nervous system excitement. Hypoglycemia stimulates adrenaline secretion after hypoglycemia. Hypoglycemia syndrome can occur. This is a compensatory response to hypoglycemia. Patients have pale faces, palpitations, cold limbs, cold sweats, hand tremor, and soft legs , Fatigue, dizziness, dizziness, hunger, panic and anxiety, etc., alleviated after eating. If the hypoglycemia gradually develops, the following clinical manifestations may appear.

2. Symptoms of unconsciousness Inhibited cerebral cortex, hazy consciousness, decreased orientation, recognition, drowsiness, sweating, tremor, impaired memory, headache, apathy, depression, dream-like state, dementia in severe cases, some people may have strangeness Behavior, etc., these neuropsychiatric symptoms are often mistaken for insanity.

3. Symptoms of epilepsy When hypoglycemia develops into the midbrain, muscle tone increases, paroxysmal seizures occur, and seizures or seizure-like seizures occur, and most of the seizures are major seizures or a state of persistent epilepsy. When the brain is involved, the patient can enter a coma, go to a state of stiff brain, bradycardia, body temperature does not rise, and various reflections disappear.

4. Symptoms of involvement of the pyramidal tract and extrapyramidal system when the subcortical center is inhibited, unconsciousness, restlessness, hyperalgesia, clonic dance movements, dilated pupils, and even tonic convulsions, extrapyramidal and pyramidal The beam sign is positive, which can be manifested as hemiplegia, paresis, aphasia, and monoplegia. These manifestations are mostly temporary damage, which can be quickly improved after giving glucose. Extrapyramidal damage can involve brain tissue structures such as pale bulbs, caudate nucleus, putamen and cerebellar dentate nucleus, which are mostly manifested as tremor, euphoria and excessive movement, torsion spasm.

5. Involvement of cerebellum Hypoglycemia can damage the cerebellum, including ataxia, uncoordinated movement, indistinguishable distance, low muscle tone and abnormal gait, etc. Especially in the late stage of hypoglycemia, ataxia and dementia often appear.

6. Cerebral nerve damage may occur when hypoglycemia, manifested as abnormal vision and visual field, diplopia, dizziness, facial paralysis, difficulty swallowing and hoarseness.

7. Peripheral nerve damage manifestations Hypoglycemia In the late stage, peripheral neuropathy often causes muscle atrophy and paresthesia, such as limb numbness, muscle weakness or tremor. Clinically, there has been clinical hypoglycemia in patients with hypoglycemic sock-type paresthesia on the distal limbs. By. There may also be peripheral stimuli and burning changes, which are related to degeneration of the spinal cord horn cells, and some people think that it is related to myositis caused by hypoglycemia caused by insulinoma. Hypoglycemic peripheral neuropathy can also cause sagging feet, failure of fine movements of hands and feet, such as being unable to write, eat, walk, or even be bedridden.

8. The appearance of hypoglycemia due to organic lesions is most common in insulinoma hypoglycemia, about 70% of which are benign adenomas, 0.5 to 3.0 cm in diameter, mostly located in the tail of the pancreas, and the pancreatic body is similar to the pancreatic head. Most of them are solitary, followed by hyperplasia, and cancers are rare. For cancers, there are more liver and adjacent tissue metastases. Domestic Hu Lixin has reported a case of multiple insulinomas, a total of 7, pancreatic head 1, pancreatic body 2, pancreatic tail 4, different sizes, diameter 10 ~ 50mm, the smallest reported as 1mm, called micro adenoma, Not easy to detect during surgery. Hypoglycemic episodes of insulinoma are severe and long-lasting, and often have the following characteristics: Hypoglycemia usually occurs on an empty stomach, such as before breakfast; Symptoms from mild to severe, from small to many, occur frequently during the onset; symptoms It is a paroxysmal attack, and the patient's condition often cannot be recalled by himself; Different patients have different symptoms of hypoglycemia, and the symptoms of the same patient are sometimes not the same; Patients with hypoglycemia often cannot tolerate hunger, Food is often added to prevent seizures before they occur, so patients generally gain weight; fasting blood glucose can be very low, sometimes only 0.56 to 1.68 mmol / L (10 to 30 mg / dl).

9. Reactive functional hypoglycemia manifestations The main manifestations of reactive functional hypoglycemia are: more common in women, milder episodes, long history, more emotional stress and history of trauma; hypoglycemic episodes are mostly 2 to 3 hours after meals Fasting blood glucose is normal or slightly lower. The symptoms of hypoglycemia are mainly increased adrenaline, which lasts for 20 to 30 minutes, often without coma, and usually relieves itself. Patients are often neurotic, obese, and have negative signs. No deterioration; Hypoglycemia is not as obvious as insulinoma, and fasting blood glucose is mostly 2.24 to 3.36 mmol / L (40 to 60 mg / dl); The patient can tolerate hunger for 72 hours without coma. Generally, the nerve cells in the brain take glucose from the bloodstream relatively constant, and it is not affected by the fluctuation of blood glucose. Therefore, the symptoms of hypoglycemia can only be shown below 45mg / dl (2.52mmol / L). The symptoms of hypoglycemia are similar to the hypoxic state of the brain, so when there is a disorder of cerebral circulation (such as arteriosclerosis, cerebral infarction), the symptoms of hypoglycemia may appear early. 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. There is no uniform standard for the threshold of blood glucose for hypoglycemia symptoms. Individual differences are large. The same is the blood glucose value of 30mg / dl (1.68mmol / L), some coma occurs, and some only have some symptoms of hypoglycemia without coma, but all need to be treated to increase blood sugar levels.

Causes of Hypoglycemia Syndrome

There are many causes of hypoglycemia. According to statistics, there can be up to 100 diseases, and other causes are still being discovered in recent years. The disease can be roughly divided into organic hypoglycemia. (Refers to the islet and extrapancreatic primary lesions caused by excessive secretion of insulin, C peptide or insulin-like substances); functional hypoglycemia (refers to patients without primary lesions, but due to nutrition and drug factors) ; Reactive hypoglycemia (referring to patients with autonomic dysfunction, vagus nerve excitement, corresponding increase in insulin secretion, resulting in clinical manifestations of hypoglycemia).

specific reason:

(1) ^[1] Insulin is not reduced in time after too much insulin is used or the condition improves.

(2) Due to conferences, outings, long-term absence of breakfast, late work, etc., the meals or extra meals are postponed more often than usual.

(3) The amount of activity was significantly increased without a corresponding meal addition or reduction in insulin consumption.

(4) Reduced food intake and did not reduce insulin accordingly.

(5) Improper injection of mixed insulin (PZI is 1 to 2 times more than RI) and the dosage is large. Often, there is a lot of urine sugar during the day and low blood sugar at night.

(6) did not eat or eat on time before the insulin action peaked.

(7) When the mood has changed from being nervous to being relaxed.

(8) After the occurrence of ketosis, the amount of insulin increases and the amount of food consumed decreases.

(9) Too much PZI.

(10) Drugs that exacerbate hypoglycemia.

Of the 10,314 autopsies, 44 (0.4%) were confirmed to be insulinomas. Normal people's blood sugar is regulated by many factors, such as the central nervous system, endocrine glands, liver, gastrointestinal, nutrition, and exercise. Glucose hormones include glucagon, epinephrine, adrenocortical hormone, growth hormone, thyroxine, and some gastrointestinal hormones. The only hypoglycemic hormone is insulin and C peptide. The rise and fall of blood glucose can also be affected by many physiological factors, such as fasting for 48 to 72 hours, strenuous exercise, drinking, breastfeeding can cause hypoglycemia, and the blood glucose of newborns and the elderly is often low. Hypoglycemia can also be caused by chronic inadequate sugar intake or malabsorption. Hepatic glycogen reserve is reduced, liver glycogenolytic enzymes are reduced, hormones that promote blood sugar are insufficient, insulin and C peptide or other hypoglycemic substances are increased, tissues consume too much blood sugar, and some poisoning factors such as salicylic acid and mushroom poisoning are all Can induce hypoglycemia syndrome. Pathogenesis: hypoglycemia mainly damages the nerves, and the brain and sympathetic nerves are the most important. In 1971, Briely discovered that hypoglycemic brain lesions are similar to ischemic cytopathies, with the basic lesions being neuronal degeneration, necrosis and glial cell infiltration. The brain's metabolic energy mainly depends on glucose, and the nerve cell's own glycogen reserve is limited, and it depends on blood glucose to supply. The various parts of the nervous system are inconsistently sensitive to hypoglycemia, with the cerebral cortex, hippocampus, cerebellum, caudate nucleus, and pale bulbs being the most sensitive. The thalamus, hypothalamus, brainstem, and cerebral nucleus are second. Finally, the anterior horn cells and peripheral nerves at the spinal cord level. Histological changes include chromatin agglutination and dissolution of the nucleus of the nerve cell, unclear nuclear membrane, swollen cytoplasm, containing small vacuoles and particles. In 1973, Chang injected mice with 2U of common insulin. After 15 to 20 minutes of sleepiness in mice, 30 to 75 minutes of myoclonus in mice, seizures, and 40 to 120 minutes into coma. The blood glucose of the drowsy mice decreased from 6.72 mmol / L (120 mg / dl) to 1.18 mmol / L (21 mg / dl), and the blood glucose level of the comatose mice was only 1.01 mmoL / L (18 mg / dl). Sugar, fat, and amino acids are the sources of energy in neurometabolism. These substances release energy after oxidation and are stored in ATP and creatine phosphate, which are released when needed. When sugar and oxygen are reduced, ATP creatine phosphate and ganglioside-binding glucose synthesis are reduced. As ATP is reduced, nucleotide synthesis is also reduced, resulting in neurological decline. The metabolism and neural function of high-energy phosphate complexes during hypoglycemia are not only related to blood glucose levels, but also closely related to partial oxygen pressure. Because of lower brain oxygen uptake during hypoglycemia, glucose uptake rate is also inhibited, and pure glucose dependence Not enough to maintain the level of oxidative metabolism, it will inevitably affect the metabolism of fatty acids and amino acids, and the level of cerebral phospholipid molecules can be reduced by 35%. When the brain tissue is hypoglycemic, the cerebral cortex is inhibited first, then the subcortical center is affected, and it spreads to the midbrain, and finally the brain is damaged and a series of clinical abnormalities occur. When blood sugar decreases, the body has a self-regulating mechanism that can stimulate adrenaline secretion, promote the breakdown of liver glycogen, and bring blood sugar back to normal levels.

Hypoglycemia Syndrome

diagnosis:

The three diagnostic criteria of Whipple's hypoglycemia syndrome are: hypoglycemia can be induced after fasting and exertion; clinical hypoglycemia can be quickly relieved by glucose; blood glucose in adults and children is often lower than 2.24 to 2.80 mmol / L (40-50 mg / dl), newborns were below 1.68 mmol / L (30 mg / dl). Idiopathic hypoglycemia often occurs in children around the age of 10. Inherited liver enzyme deficiency, Reye syndrome hypoglycemia is also more common in childhood. Insulinoma mostly occurs in patients aged 13 to 57 years. The incidence ratio of male to female is 5: 1. Such patients often do not tolerate hunger and have a habit of eating more. Therefore, there are many obese people, and the patient's previous health foundation is good, which helps Differential diagnosis.

Laboratory inspection:

1. Fasting blood glucose should be measured multiple times, and the hypoglycemia level is 3.36mmol / L (60ng / dl).

2. Glucose tolerance test Hypoglycemia patients and insulinoma patients mostly showed hypoglycemia curve. Occasionally normal values, hypoglycemia occurs only at the onset.

3. Serum insulin and C-peptide determination The serum insulin and C-peptide values are commonly measured by radioimmunoassay. The normal values are (14 ± 8.7) U / ml, and the C-peptide value is 0.8 to 4.0 ng / ml. The insulin value of patients with insulinoma increased to 160 U / ml and the C-peptide value increased accordingly.

4. Fasting test: Fasting for 24 hours, blood glucose decreased, hypoglycemia symptoms, patients with insulinoma can not tolerate, and a series of symptoms of hypoglycemia, the test should be ended as soon as possible, not to cause coma to prevent brain damage.

5. Tolubutamide (D860, Tolbutamide) test After intravenous injection of D8601g, the insulin rise can reach 100u / ml 15 20h, and the hypoglycemic level can be caused within 2 3h thereafter, which can cause severe hypoglycemia in patients, and should be stopped if necessary To test, administer glucose. Functional hypoglycemia response was normal, and the blood glucose of patients with insulinoma decreased significantly.

6. Leucine test is a challenge test. Intravenous injection of 150 mg of leucine and a drop in blood glucose of more than 1.4 mmol / L (25 mg / dl) indicate insulinoma. L-leucine 200mg / kg body weight, blood glucose and insulin were measured before oral administration and 10, 20, 30, 40, 50, 60 minutes after taking, respectively, because leucine can stimulate insulin secretion

With release, taking the drug for 30 to 45 minutes, the blood glucose dropped below 50 mg / dl (2.8 mmol / L) as a positive reaction.

7. Glucagon test is a challenge test. After 6-8 hours of eating, intramuscular injection of glucagon 1mg, normal people's blood glucose reached a peak in 45 minutes, and returned to normal in 2 hours. Patients with hypoglycemia have a peak blood glucose that appears early and are still at a significantly lower blood glucose level within 2 hours. Patients with insulinoma have a peak insulin response above 130 U / ml when glucagon is administered intravenously for 5 to 30 minutes. Normal people and non-obese people are not more than 100U / ml. Blood must be collected every 5 minutes for 30 minutes to get a correct conclusion.

Other auxiliary checks:

1. EEG is similar to hypoxia, without specific changes, showing slow waves or other changes. Long-term hypoglycemia may have abnormal changes in patients with brain lesions.

2. The EMG nerve conduction time is normal. The distal muscles showed denervation and the number of motor unit potentials decreased. Diffuse denervation fibers, electrical discharges at the tip and giant motor units, polyphasic potentials. More consistent with changes in peripheral neurons or anterior horn cell types.

3. X-ray examination occasionally calcified adenomas, distortion or displacement of adjacent organs. Pancreatic arteriography showed increased blood flow. Selective superior mesenteric artery and celiac arteriography are helpful for localization of lesions.

4. CT and MRI scans can find space-occupying lesions in the abdominal cavity and pancreas.

5. B-ultrasound can find tumors in the pancreas. Those less than 1cm are easily missed and not as reliable as CT and MRI.

6. Other pancreatic radionuclide scans, ECT scans, and 75Se-methionine examination can find space-occupying lesions inside and outside the pancreas.

Differential diagnosis of hypoglycemia syndrome

There are many differential diagnoses of hypoglycemia syndrome. Pay attention to:

Individual differences in elderly patients with mild, mild, and arteriosclerosis patients;

Patients with hypohypophysis, adrenal cortex dysfunction, and hypothyroidism;

diabetic mothers;

Severe hepatitis and nephritis;

Concomitant use of hypoglycemic drugs, such as Baotaisong, sulfaisoxazole, chloramphenicol and dicoumarin, can strengthen the action of D860, stimulate insulin secretion and lower blood sugar.

The accuracy rate of diagnosing hypoglycemia according to the Whipple triad can reach 91%, and combined with medical history, blood glucose and serum insulin determination can improve the diagnostic level. Generally, D860, L-leucine and glucagon tests are rarely used in clinical practice. Various tests can be done selectively, commonly used OGTT + insulin release test and fasting test. Normal human pancreatic cells release different amounts of insulin under the stimulation of different factors. The order of least is glucose tolerance test> D860 test> glucagon test> leucine test, and the order of insulinoma is pancreatic high Glycan test> D860 test> Leucine test> Glucose tolerance test, the sensitivity to glucose is low. Differential diagnosis should be made with epilepsy, syncope, brain tumors, diabetic ketoacidosis, coma, hypoparathyroidism, cerebrovascular accident, uremia, hysteria, and hepatogenic coma.

Treatment options for hypoglycemia syndrome

medical treatement

The cause should be treated. Detection of insulinoma should be surgically removed. Before surgery, hydrocortisone or prednisone (prednisone), phenothiazide glycemic drugs such as diazoxide or trichlormethiazide can be used. Malignant pancreatic tumors can use streptozotocin to destroy islet cells and relieve hypoglycemia. The usage is 20-30mg / kg body weight, intravenous drip, once a week for a total of 8-10 times, the total dose is 8 9g. Another method is to inject streptozotocin directly into the abdominal cavity, 15 to 40 mg / kg body weight, once every 2 days, 5 to 10 times as a course of treatment. It should pay attention to liver, kidney and gastrointestinal damage during administration. The side effects are Nausea and vomiting account for about 94%, renal toxicity is 65%, liver toxicity is 67%, and hematological toxicity is 20%. For pancreatic hyperplasia cases, pancreatic glands and pancreatic tails should be removed. Insulin hyperplasia cases, postoperative complications include pancreatic fistula, followed by pseudopancreatic cysts, diabetes, and acute pancreatitis. Hypoglycemia caused by extrapancreatic tumors is generally thought to be caused by ectopic insulin secretion.

In 1989, David and others reported that fibrosarcoma can secrete a plasmainsulin-like growth factor II (IGF-), which can continuously inhibit growth hormone secretion, increase insulin secretion and cause hypoglycemia, and the treatment should be to remove extrapancreatic tumors. Diphenylamide (DPH) can inhibit insulin secretion, but can cause elevated blood sugar, urine glucose positive, can aggravate diabetes, and is beneficial for insulinoma or reactive hypoglycemia. Functional hypoglycemia has fast absorption after giving sugar. Oral hypoglycemic drugs are effective for some mild diabetic hypoglycemia, which can make the increase and decrease of insulin secretion correspond to the rise and fall of blood glucose levels. Iatrogenic hypoglycemia should be based on prevention to reduce the inappropriate application of hypoglycemic drugs and other drugs, especially the elderly diabetic patients should reduce the application of glibenclamide (hypoglycemic) to avoid hypoglycemia. Ketopathic hypoglycemia should avoid fatty foods and give high-protein and high-sugar diets. Leucine-sensitive hypoglycemia should be given a low-protein diet and a carbohydrate diet containing a minimum amount of leucine. Adrenaline, glucagon, and low-dose ACTH preparations can be used at the same time. Hereditary fructose intolerance to hypoglycemia should be avoided in foods that are high in fructose. Liver-derived hypoglycemia should be based on hepatoprotective therapy, and a high-sugar and high-protein diet should be used. Endocrine disease hypoglycemia mainly treats the primary disease and reduces the incidence of hypoglycemia. Onset of hypoglycemia, light patients can be relieved by quickly taking a sugary diet, and those who cannot take it orally should quickly inject a 50% glucose solution 40 to 60ml, and then increase the sugary diet. Hypoglycemic coma, intravenous injection of 50% glucose solution 60 to 100ml, and then intravenous drip of 10% glucose solution 1000ml, to maintain blood glucose at 150-300mg / dl, that is, 8.4-16.8mmol / L; Glucagon can be given 1mg Or 2 mg, once every 2 hours, intramuscular injection or intravenous injection; 30 mg prednisone (prednisone), once every 6 hours to stabilize blood sugar; supplement 300 g carbohydrate diet daily until blood sugar stabilizes to normal Level. People with functional hypoglycemia should be provided with mental comfort, physical exercise, low-dose stabilizers, anticholinergic drugs such as bromprolide (probencin), atropine, etc. to ease the intestinal absorption rate of food and Reduce insulin secretion.

1. Cure As far as hypoglycemia can be cured, blood sugar can rise back to normal levels. Hypoglycemic encephalopathy is a sequelae of hypoglycemia and cannot be cured. Insulin tumors can be cured after surgery. Patients with pancreatic hyperplasia type hypoglycemia may be partially cured after surgery and some may develop diabetes. Hereditary diseases are currently incurable.

2. Improved Although most patients with hypoglycemia are treated, they still have hypoglycemia and become relapsed.

3. Ineffective Some patients with malignant tumor hypoglycemia often have seizures, even coma, and have a poor prognosis.

Prognosis and prevention of hypoglycemia syndrome

Prognosis:

Related to the etiology, functional hypoglycemia, islet -cell tumors, drug-induced hypoglycemia, early diabetes and hypoglycemia generally have a good prognosis, and congenital enzyme defects and malignant tumor hypoglycemia have a poor prognosis. Postoperative complications have the worst prognosis with acute necrotizing pancreatitis, which can lead to death. There is still a possibility of recurrence after tumor resection, and follow-up observation should be performed. Patients with hypoglycemia can cause hypoglycemia encephalopathy, peripheral neuropathy, etc. after repeated relapses, resulting in lifelong disability and even death. Therefore, patients with hypoglycemia should be diagnosed as early as possible and treated in time to strive for cure. If the diagnosis is not timely, delaying treatment can cause disability and death.

prevention:

(1) Reasonable use of insulin. Insulin is divided into long-acting, intermediate-acting, and short-acting according to its duration of action. It is best to ask the doctor to help rational adjustment of the insulin dose according to the condition and food intake. In addition to the dose, pay attention to the duration of action. With ordinary insulin, medication should be taken 15 minutes before eating, but not earlier than 30 minutes before eating, otherwise hypoglycemia may occur. If you use medium- or long-acting insulin, you should ask your doctor to pay attention to the time when insulin is strongest. It should not be placed on an empty stomach at night, otherwise nightly hypoglycemia may occur. If you use short-acting and medium-long-acting insulin, you should pay more attention to the strongest action time of the overlapping effects of the two, not on fasting or at night, so as to avoid hypoglycemia, pay attention to clearing the highest blood sugar, and you can't rule out the night hypoglycemia.

(2) Patients injected with mixed insulin should pay special attention to eating dinner on time and adding small meals before going to bed late to prevent hypoglycemia at night. Patients who are prone to hypoglycemia in the middle of the night and early morning should eat more staple foods or slowly absorbed protein-rich foods such as eggs and dried tofu before going to bed late.

Precaution

(3) Make a record of the condition observation. If urine glucose is negative for several consecutive days, consider reducing insulin dosage as appropriate, and add meals in time before the moment when insulin action is strongest and when there is a lot of activity.

(4) When the amount of labor is increased or the activity is excessive, reduce the amount of insulin or add meals in time. Patients taking oral hypoglycemic drugs should also reduce the dosage or add meals in time.

(5) Always pay attention to diet, which should respond to the role of insulin, pay special attention to observe changes in urine glucose, and add meals in time before the moment when insulin action is the strongest.

(6) All people with diabetes should always carry fruit candy and cookies with them in order to correct the hypoglycemic reaction at any time.

(7) Introduce some knowledge about diabetes and hypoglycemia to family members and surrounding comrades, so that they have a better understanding of the symptoms and treatment of hypoglycemia, so as to deal with hypoglycemia in time.

(8) Among oral hypoglycemic agents, especially hypoglycemic agents have a higher chance of causing hypoglycemia, and precautions should be taken. It should be started in small doses, taken once a day, up to twice a day, and the dose should be small at night.

(9) The patient should carry a hard card with the patient's name, diagnosis, disease description, unit address, home address and phone number, so that when hypoglycemia occurs, people can take care of it according to the information on the card.

Hypoglycemia Syndrome Emergency Measures

1. Absolute bed rest and rapid glucose supplementation is the key to determining prognosis. Timely sugar supplementation will completely relieve the symptoms; delayed treatment will cause irreversible brain damage. Therefore, it should be emphasized that at the time of the onset of hypoglycemia, any substance with higher sugar content, such as biscuits, juice, etc., should be given immediately. Severe cases should pay attention to inhaling food into the lungs and inhaling the trachea, which may cause aspiration pneumonia or atelectasis.

2. Patients with hypoglycemia who can eat on their own should eat low sugar, high protein, high fat, eat less and eat more, and drink sugar at midnight if necessary.

3. Intravenous bolus 50% glucose 40-60ml is the most commonly used and effective method for rescue of hypoglycemia. If the condition is not serious and has not caused serious brain damage, the symptoms can be quickly relieved and the mind can be immediately sober.

Patients with conditions should immediately measure with a blood glucose meter. Those with blood sugar less than 3.8 mmol / L should be quickly supplemented with carbohydrate-containing foods, such as half a cup of sweet juice, half a cup of sugar water, 1 tablespoon of honey, and 3 to 5 pieces. Biscuits, 3 to 4 cubes of sugar, 2 to 3 candies, etc. After 10 to 15 minutes, if the symptoms have not disappeared, you can take it again. If the symptoms disappear, but there is more than an hour before the next meal, add a staple food, such as 1 slice of bread, a bun, 3 to 5 biscuits, etc. In case of unconsciousness or sudden coma, the family members should send the patient to the hospital as soon as possible.