What Is the Connection Between Dehydration And Diabetes?

Diabetes is a group of metabolic diseases characterized by hyperglycemia caused by genetic, environmental, immune and other factors, which are caused by defects in insulin secretion and / or disorders of its biological function. Its acute complications refer to acute metabolic disorders of diabetes, including diabetic ketoacidosis, hypertonic non-ketogenic diabetic coma, and lactic acidosis and hypoglycemic coma during the treatment of diabetic hypoglycemia.

Chen Lulu

(Chief physician)

Department of Endocrinology, Wuhan Union Medical College Hospital

Diabetes is a group of metabolic diseases characterized by hyperglycemia caused by genetic, environmental, immune and other factors, which are caused by defects in insulin secretion and / or disorders of its biological function. Its acute complications refer to acute metabolic disorders of diabetes, including diabetic ketoacidosis, hypertonic non-ketogenic diabetic coma, and lactic acidosis and hypoglycemic coma during the treatment of diabetic hypoglycemia.

Western Medicine Name

Acute complications of diabetes

Affiliated Department

Internal Medicine-Endocrinology

Multiple groups

Diabetics

Contagious

Non-contagious

Acute complications of diabetes ketoacidosis

Causes of acute complications of diabetes

The cause of DKA in patients with type 1 diabetes is mostly due to interrupted insulin or insufficient insulin consumption. Most patients with type 2 diabetes are due to stress factors such as infection, trauma, and medication. DKA can also occur in insulin-treated patients with type 1 diabetes under stress. The common causes are:

(1) Infection: Respiratory infections are the most common, such as pneumonia and tuberculosis. Urinary system infections such as acute pyelonephritis, cystitis, etc., in addition to appendicitis, peritonitis, and pelvic inflammatory disease.

(2) Acute myocardial infarction, heart failure, cerebrovascular accident, trauma, surgery, anesthesia and severe mental stimulation.

(3) Pregnancy: Especially in the second half of pregnancy, due to the significant increase in the demand for insulin, ketosis or even ketoacidosis may be induced.

(4) Others: the application of certain drugs such as glucocorticoids, and certain diseases such as Cushing's disease, acromegaly, and glucagonoma. ^[1]

The pathogenesis of acute complications of diabetes

(A) hormone abnormalities

In recent years, scholars at home and abroad generally believe that the cause of DKA is due to the abnormality of multiple hormones, which disrupts the dynamic balance of hormone secretion and fat metabolism disorders. DKA characterized by hyperglycemia, hyperketones, and metabolic acidosis has appeared. Its mechanism is mainly insufficient absolute or relative secretion of insulin; excessive secretion of glucagon; elevated levels of other anti-regulatory hormones such as epinephrine, growth hormone and cortisol.

(Two) metabolic disorders

In the physiological state, the metabolism of sugars, fats, blood ketones, electrolytes, water and other substances in the body is under the precise regulation of the neuroendocrine system, maintaining a dynamic balance. Insulin, as an energy storage hormone, plays a role in metabolism Promote synthesis and inhibit decomposition. When the insulin secretion is absolute or relatively inadequate, the absolute or relative increase of insulin-antagonizing hormones promotes the metabolic breakdown in the body, inhibits synthesis, causes glucose metabolism disorders, accelerates the breakdown of fats and proteins, inhibits synthesis, increases fat mobilization, and ketone bodies. Increased production eventually leads to DKA.

Pathophysiology of acute complications of diabetes

(A) acidosis

Beta-hydroxybutyric acid, acetoacetic acid, and proteolytic organic acids are increased, cycle failure, and renal excretion of acidic metabolites are reduced, leading to acidosis. Acidosis can reduce insulin sensitivity; increase tissue breakdown and potassium escape from cells; inhibit tissue oxygen utilization and energy metabolism. Severe acidosis worsens microcirculatory function, reduces myocardial contractility, and leads to hypothermia and hypotension. When the blood pH drops below 7.2, it stimulates the respiratory center to cause deepening of breathing; when it is as low as 7.1 to 7.0, it can inhibit the function of the respiratory center and central nervous system and induce arrhythmia.

(Two) severe dehydration

Severe hyperglycemia, hyperketones, and various acidic metabolites cause osmotic diuresis. A large number of ketone bodies are excreted from the lungs and take away a large amount of water. Anorexia, nausea, and vomiting reduce the amount of water and cause extracellular water loss; plasma As the osmotic pressure increases, water is transferred from the inside to the outside of the cell causing intracellular water loss.

(Three) electrolyte balance disorders

Osmotic diuresis simultaneously causes a large loss of sodium, potassium, chlorine, phosphate, etc. Anorexia, nausea, and vomiting reduce electrolyte intake and cause electrolyte metabolism disorders. Insulin has insufficient effects, increased decomposition of substances and reduced synthesis, and potassium ions (K +) escape from the cells, leading to intracellular potassium loss. Due to blood concentration, potassium retention when renal function declines, and potassium transfer from intracellular to extracellular, the potassium concentration in the blood can be normal or even increased, which masks serious potassium deficiency in the body. With the replenishment of blood volume (dilution effect) during treatment, urine output increases, potassium excretion increases, and acidosis is corrected and potassium is transferred into cells with insulin, severe hypokalemia can occur, induce arrhythmias, and even cardiac arrest .

(D) carrying oxygen system disorders

The ability of red blood cells to supply oxygen to tissues is related to the affinity of hemoglobin and oxygen, which can be reflected by the blood oxygen dissociation curve. The increase of erythrocyte glycated hemoglobin (GHb) and the decrease of 2,3 diphosphoglycerate (2,3-DPG) during DKA increased the affinity of hemoglobin and oxygen, and the blood oxygen dissociation curve shifted to the left. In the case of acidosis, the blood oxygen dissociation curve shifts to the right, and the release of oxygen increases (Bohr effect), which plays a compensatory role. If acidosis is corrected too quickly, this compensatory effect is lost, while blood GHb is still high, and 2,3-DPG is still low, which can increase tissue hypoxia and cause organ dysfunction, especially brain hypoxia, which leads to brain damage. Edema is the most important.

(5) Peripheral circulatory failure and renal dysfunction

Severe dehydration, decreased blood volume, and failure to correct microcirculation disorders can lead to hypovolemic shock. Decreased renal perfusion volume causes oliguria or anuria, and acute renal failure occurs in severe cases.

(6) Central nervous system dysfunction

Severe acidosis, dehydration, hypoxia, systemic circulation, and microcirculation disorders can lead to dehydration or edema of brain cells and central nervous system dysfunction. In addition, improper treatment, such as correcting acidosis, may lead to an abnormal increase in cerebrospinal fluid acidosis, excessive blood glucose drop or excessive infusion, and imbalance of osmotic pressure may cause secondary cerebral edema and worsen central nervous system dysfunction. . ^[2]

Clinical manifestations of acute complications of diabetes

Extremely thirsty, excessive urine, marked dehydration, extreme fatigue, nausea, vomiting, and low appetite. A small number of patients show non-fixed pain in the whole abdomen, sometimes more severe, like surgical acute abdomen, but no abdominal muscle tension and mild tenderness ,headache. Loss of spirit or irritability, fainting consciousness, and finally drowsiness and coma; deep breathing during severe acidosis, unpleasant frequency, no dyspnea, and bad apple smell on exhalation. Different degrees of dehydration, sunken eyes, poor skin elasticity, fast pulses, low or low blood pressure, and dryness of the tongue are important and sensitive signs for estimating the degree of dehydration. In addition, there are still symptoms of the cause, such as infection, heart and brain Signs and symptoms of vascular disease.

Diagnosis and diagnosis of acute complications of diabetes

Laboratory inspection:

(1) The blood sugar and hyperglycemia are mostly 16.7 ~ 33.3mmol / L, and sometimes it can reach more than 55mmol / L.

(2) Ketone body and blood ketone body> 4mmol / L. Urinary ketone body was positive. Acetone has no renal threshold. If there are too many ketone bodies and renal function is not impaired, although urinary ketones are positive, blood ketones are not high, and clinically, there is no ketoneemia. In other words, renal function is mostly reduced in diabetic ketoacidosis.

(3) The plasma CO2 binding force is reduced by 30 volumes, or less than 90%, and the plasma pH is <7.35.

(4) Blood gas analysis standard hydrogen carbonate and buffered alkali are lower than normal, the residual negative value of alkali increases, and the anion gap is> 16.

Diagnosis and differential diagnosis

Early diagnosis is the key to determining the success of treatment. Clinically, for patients with unexplained nausea and vomiting, acidosis, dehydration, shock, and coma, especially those who have a rotten apple smell on their breath, low blood pressure, and high urine output, with or without Diabetes history should be thought of this disease.

Differential diagnosis includes: (1) other types of diabetic coma: hypoglycemia coma, hyperglycemia and hypertonic state, lactic acidosis. (2) Coma caused by other diseases: meningitis, uremia, cerebrovascular accident, etc. Some patients take DKA as the first manifestation of diabetes, and some cases are mainly complained of other diseases or predisposing factors. Some patients have more complicated conditions such as coexistence of DKA with uremia or stroke, and should be distinguished.

Treatment of acute complications of diabetes

Rehydration as soon as possible to restore blood volume. Correct water loss, reduce blood sugar, correct electrolyte and acid-base balance imbalance, and actively seek and eliminate incentives, prevent complications, and reduce mortality.

(I) Rehydration: It is especially important for severe DKA, which is not only conducive to the correction of dehydration, but also helps to reduce blood sugar and eliminate ketone bodies.

(1) Total fluid replacement: Generally estimated at 10% of the patient's weight (kg), the adult DKA usually loses 4-6L of water.

(2) Types of fluid replacement: Start with normal saline. If the blood glucose is not severely increased at the beginning of the infusion or after the blood glucose drops to 13.9mmol / L after treatment, 5% glucose or sugar saline should be input to eliminate ketosis.

(3) fluid replacement speed: the principle of fast first and then slow. In principle, input 1/3 to 1/2 of the total water loss in the first 4h, and input about 4000ml in the first 12h, which is 2/3 of the total infusion. The rest is made up within 24-28 hours.

(Two) insulin treatment

Low-dose insulin therapy, infusion of insulin 0.1U / (kg · h), the blood concentration can reach 120U / ml, this concentration can have the largest inhibitory effect on ketone body production, and can effectively reduce blood. During the medication process, blood glucose should be closely monitored if the blood glucose does not drop or the drop is not obvious, especially in patients with concurrent infection or original insulin resistance.

(3) Correct electrolyte and acid-base balance imbalance

Generally, after infusion and insulin treatment, acidosis can be corrected by decreasing ketone body levels, and alkali supplementation is generally unnecessary. Indications for alkali supplementation were blood pH <7.1 and HCO3- <5mmol / L. Isotonic sodium bicarbonate solution should be used, and alkali replenishment should not be too fast.

Potassium supplementation should be based on blood potassium and urine volume: before treatment, the blood potassium level is lower than normal, and potassium supplementation should be started immediately. For the first 2 to 4 hours, potassium supplementation is about 13-20 mmol / L per hour through intravenous infusion; / h, potassium supplementation also started immediately; blood potassium was normal. If the urine output is less than 30ml.h, potassium supplementation will be suspended. After the urine volume increases, potassium supplementation will be started. If the potassium level is higher than normal, potassium supplementation will be suspended. During the treatment, the blood potassium and urine volume shall be measured regularly, and the potassium supplementation amount and speed shall be adjusted. Oral potassium should be continued for several days after recovery.

4. Symptomatic treatment: treatment for infection, heart failure, arrhythmia, etc.

In addition, care should be taken during treatment

(1) The large dose of insulin during treatment can easily cause the blood glucose to drop too quickly, leading to a sudden decrease in plasma osmotic pressure, while the intracellular state is still hypertonic, resulting in a large intra- and extracellular osmotic pressure difference. Causes water molecules to rapidly diffuse into the cell, causing cell edema, which is not conducive to cell function recovery.

(2) Closely observe the changes in the condition during treatment, regularly detect changes in vital indicators and blood glucose, osmotic pressure, and CO2 binding power, and deal with them in a timely manner.

(3) Clinical care should be strengthened during coma. Prevent the occurrence of unexpected complications.

(4) Anti-infective treatment should be given in a timely manner according to the patient's general condition and blood picture.

Prognosis of acute complications of diabetes

After timely rescue treatment of DKA, the prognosis is mostly good. Type 1 diabetic ketoacidosis should be particularly cautious and active treatment measures must be taken. In case of concurrent renal failure, heart failure, or multiple system and multiple organ failure, the prognosis will depend on the number of failed organs. The greater the number of failed organs, the worse the prognosis. If ketoacidosis is not treated in time, its prognosis is mostly poor.

Prevention of acute complications of diabetes

(1) Diabetes treatment should be reasonable to prevent and control blood sugar spikes. Changes in rapid decline, maintaining blood glucose below 11.20mmol / L.

(2) The diet of diabetic patients should be regular, prevent overeating, and control the diet according to the diabetes diet standard.

(3) Pay attention to psychological balance, and avoid excessive mental and emotional excitement.

(4) Prevent various infections, maintain physical strength, and avoid fatigue.

(5) Proper physical activity according to physical conditions.

Nursing care for acute complications of diabetes

Good care is an important part of rescuing DKA. The mouth and skin should be cleaned on time to prevent pressure ulcers and secondary infections. Carefully observe the changes in the condition, accurately record the state of mind, pupil size and response, vital signs, and the amount of water flowing in and out. Blood glucose is measured every 1 to 2 hours, and ketones, creatinine, electrolytes, and acid-base balance indicators are reviewed every 4 to 6 hours. ^[3]

Acute complications of diabetes

Causes of acute complications of diabetes

1. Stress and infections such as cerebrovascular accidents, acute myocardial infarction, acute pancreatitis, gastrointestinal bleeding, trauma, surgery, heat stroke or hypothermia. Infections, especially upper respiratory tract infections and urinary tract infections, are most often induced.

2. Insufficient water intake decreases the sensitivity of the thirst of the elderly, bedridden patients, patients with mental disorders or coma, and young children who cannot actively take water.

3. Excessive dehydration and dehydration, such as severe vomiting, diarrhea, patients with large area burns, neurological and surgical dehydration treatment, dialysis treatment, etc.

4. High-sugar intake and input, such as a large intake of sugary drinks, high-sugar foods, intravenous infusion of a large amount of glucose when the diagnosis is unknown or missed, complete intravenous hypertrophy, and the use of sugary solutions for hemodialysis or peritoneal dialysis. Happening. Especially in patients with certain endocrine diseases combined with glucose metabolism disorders, such as hyperthyroidism, acromegaly, cortisol, and pheochromocytoma are more likely to be induced.

5. Drugs Many drugs can be incentives, such as the heavy use of diuretics such as glucocorticoids, thiazines or furosemide (fast urine), propranolol, phenytoin, chlorpromazine, cimetidine, glycerol , Azathioprine and other immunosuppressants. Both can cause or aggravate the body's insulin resistance and increase blood glucose and dehydration. Some drugs, such as thiazide diuretics, can also inhibit insulin secretion and reduce insulin sensitivity, which can induce HNDC.

6. Others such as acute and chronic renal failure, diabetic nephropathy, etc., because the glomerular filtration rate decreases, the clearance of blood glucose also decreases.

The pathogenesis of acute complications of diabetes

The pathogenesis of this disease is complex and has not been fully elucidated. The basis of the disease is patients with varying degrees of glucose metabolism disorders. The basic causes are insufficient insulin, target cell dysfunction, and dehydration. Under the influence of various incentives, the original glucose metabolism disorder is aggravated, the response of the islets to sugar stimulation is reduced, insulin secretion is reduced, liver glycogen breakdown is increased, blood glucose is significantly increased, severe hyperglycemia and diuresis cause osmotic diuresis, As a result, a large amount of water and electrolytes are lost from the kidneys. Because patients often have active intake dysfunction and varying degrees of renal impairment, hyperglycemia, dehydration, and high plasma osmotic pressure gradually increase, eventually leading to HNDC status.

HNDC and ketoacidosis are both acute complications of diabetes due to insufficient insulin. Both have hyperglycemia, dehydration, and varying degrees of electrolyte loss, but the clinical manifestations between typical HNDC and typical ketoacidosis It's different. Generally speaking, the former is more common in middle-aged and elderly people. Hyperglycemia, dehydration and high plasma osmotic pressure are more severe than ketoacidosis, but there is often no or only mild ketoacidosis; the latter is more common in younger people. Type 2 diabetes, hyperglycemia, and dehydration are mild, but there are often moderate or severe ketoacidosis, and the mechanisms that cause these differences between HNDC and ketoacidosis have not been fully elucidated. Currently thinks:

1. HNDC patients have relatively high insulin secretion, which is sufficient to inhibit the breakdown of fat and the production of ketone bodies, but cannot prevent the increase of blood sugar caused by other causes. It is also believed that there is no significant difference between the two, and that plasma insulin levels in some HNDC patients appear unpredictable.

2. Plasma growth hormone and catecholamine levels in patients with HNDC are lower than ketoacidosis, and both of these hormones have a strong role in promoting lipolysis and ketone body production. However, some people believe that there is no significant difference between the two hormones.

3. HNDC patients are severely dehydrated, and severe dehydration is not conducive to the production of ketone bodies. Older people have less water reserves than younger patients, and often have reduced thirst central sensitivity and renal insufficiency. Severe acidosis. -oxidation of fatty acids and the formation of ketone bodies require the participation of water, so severe dehydration can affect the production of ketone bodies. In addition, severe dehydration can cause blood concentration, impaired glucose excretion by the kidneys, and cause more severe hyperglycemia.

4. Patients with HNDC have ketogenic dysfunction in the liver, and their ability to reduce glucose is reduced, resulting in high blood sugar and mild ketosis. Normal people can excrete 20 g of glucose from the urine per hour in a hyperglycemic state, so the blood glucose of a person with normal renal function generally does not exceed 27.8 mmol / L (500 mg / dl). About 90% of patients with this disease are accompanied by kidney disease, dysfunction of glucose, and severely increase blood sugar.

5. Severe hyperglycemia may have an antagonistic effect on ketone body production. Clinically, it can often be found that patients with HNDC have severe hyperglycemia without obvious ketoacidosis, and patients with ketoacidosis have significant ketoacidosis. Poisoning and relatively low blood glucose levels. This phenomenon may be: in patients with HNDC under high glucose and dehydration, ketone production in the liver is inhibited; in patients with ketoacidosis, a large amount of fatty acids are oxidized to generate ketone bodies, and the plasma NAD / NADH ratio decreases. The level of alanine necessary for gluconeogenesis is reduced, thereby inhibiting the effects of liver gluconeogenesis.

Clinical data show that HNDC and ketoacidosis are not two distinct symptoms. There are a variety of intermediate types between them, forming a continuous pathological spectrum, and the two are the two extremes of this continuous disease spectrum. That's it. In clinical, HNDC also has significant ketoacidosis, while typical ketoacidosis also has a hypertonic state. It can be seen that there can be a large overlap between HNDC and ketoacidosis, which is called Overlap syndromes, such as typical ketoacidosis, cannot deny the diagnosis of HNDC; severe hyperglycemia and hypertonic state can sometimes be seen in patients with ketoacidosis, which should be taken seriously in clinical work.

Pathophysiology of acute complications of diabetes

Normal plasma osmotic pressure is maintained at 280-300 mmol / L, which is mainly provided by blood Na +, but it will also cause plasma osmotic pressure to increase when blood glucose is significantly increased. In HNDC, hyperglycemia and high urine glucose cause osmotic diuresis. About 50% of urinary osmotic pressure is maintained by glucose in the urine. Therefore, patients with water loss are often far more severe than electrolyte loss, and the average water loss is 9L (24% The total amount of water in the body), on the one hand, dehydration can increase the secretion of cortisol, catecholamines and glucagon; on the other hand, it can further suppress the secretion of insulin, continue to increase hyperglycemia, and form a vicious circle. In addition, dehydration can also increase secondary aldosterone secretion, increase hypernatremia, increase plasma osmotic pressure, and dehydrate brain cells, leading to prominent neuropsychiatric symptoms of this disease.

Clinical manifestations of acute complications of diabetes

Multiple groups

Elderly people, most often in the age of 50 to 70, the prevalence of men and women is about the same. About half are known to have diabetes, and most are type 2 diabetes patients, about 30% have a history of heart disease; about 90% have kidney disease.

Disease symptoms

Prodromal phase-a period before the onset of neurological symptoms and coma. This period ranges from several days to several weeks. Half of the patients have no history of diabetes and most have a history of decreased kidney function. Due to fatigue, relaxed diet control, and increased chances of infection, the incidence is higher in winter, especially around the Spring Festival. The onset of the patient is slow, mainly manifested by the exacerbation of the original diabetic symptoms, such as irritability, polydipsia, polyuria, fatigue, dizziness, loss of appetite, nausea, vomiting, abdominal pain, etc., unresponsiveness and apathetic expression. Note: Some patients lack thirst that is compatible with the degree of dehydration. This is because diabetic non-ketotic hyperosmolar coma is more common in the elderly, and the elderly often have arteriosclerosis, the thirst center is not sensitive, and the hypertonic state is also Can make hypothalamic central dysfunction.

Typical period-if the prodromal period is not treated in time, the condition continues to develop, due to severe dehydration caused by plasma hyperosmosis and decreased blood volume, patients mainly show severe dehydration and nervous system symptoms.

(1) Severe dehydration, often accompanied by circulatory failure: significant weight loss, dry skin, mucous membranes, lips and tongue, soft, swollen eyes, oliguria, etc., and blood pressure often decreases. In severe cases, there may be symptoms of peripheral circulation failure. The pulse is fine and fast, the pulse compression is small, the jugular vein is incomplete in the supine position, hypotension occurs in the standing position, and even the limbs are cold, and the cyanosis is in shock. Some suffer from oliguria and anuria due to severe dehydration.

(2) Nervous system dysfunction: 50% of consciousness and 30% of coma. Reversible local nervous system signs such as local or generalized epilepsy (13% -17%), myoclonus , Hemianopia, paresis, hallucinations, aphasia, and pathological reflexes (23% to 26%). The performance of the nervous system is related to the rate and degree of increase in plasma osmotic pressure and has little to do with acidosis. Those with a high degree of hypertonicity or developing rapidly are prone to the manifestation of central nervous system dysfunction.

Symptoms and signs associated with the onset-patients may have symptoms of hypertension, kidney disease, coronary heart disease, etc .; symptoms of induced diseases such as pneumonia, urinary system infection, pancreatitis; complications of cerebral edema, thrombosis, vascular embolism, etc. . The patient's body temperature is usually normal or slightly elevated. If the body temperature decreases, it may indicate that it may be accompanied by acidosis and / or sepsis, and it should be paid enough attention. If the body temperature is above 40 ° C, it may be central high fever, and it may also be caused by various factors. Caused by infection.

3. Disease hazards

Complicated lung infections are most common after HNDC, and the risk of thrombosis is significantly increased due to severe dehydration. Due to extreme hyperglycemia and high plasma osmotic pressure, blood is condensed and viscosity increased, and arterial and venous thrombosis is easy to occur, especially cerebral thrombosis, which leads to higher mortality. HNDC patients may have cerebral cortex or subcortical damage caused by dehydration, blood concentration, or vascular embolism. Most of these changes can be reversed or returned to normal after effective treatment. There are also a few symptoms that can still leave some neurological and mental disorders within a period of time after HNDC correction.

Diagnosis and diagnosis of acute complications of diabetes

The diagnosis of HNDC is not difficult. The key problem is to improve the understanding of the disease. The possibility of the disease should be thought of in a comatose patient. If middle-aged and elderly patients are found to have significant mental disorders and severe dehydration, deep breathing with unknown causes should be more vigilant and necessary examinations should be conducted in time to detect the disease. Regarding the laboratory diagnosis basis of HNDC, some people abroad have proposed the following standards: blood glucose 33mmol / L (600mg / dl). Effective plasma osmotic pressure is 320mmol / L. serum [HCO3] 15mmol / L or arterial blood gas examination pH 7.30 [4]. It is worth noting that there are individual cases with diabetic ketosis overlap syndrome. Therefore, positive urine ketone bodies, obvious acidosis, or blood glucose lower than 33 mmol / L, cannot be used as a negative basis for the diagnosis of HNDC. However, patients with HNDC have obvious hypertonic state. If the effective osmotic pressure of plasma in coma patients is less than 320mmol / L, the possibility of other diseases that cause coma should be considered. Some patients have high blood glucose, but due to low blood sodium, the effective osmotic pressure does not reach 320mmol / L. Although these patients cannot diagnose HNDC, they should still be treated as HNDC.

HNDC should be distinguished from certain diseases:

(1) Hypertonic state caused by other reasons, such as dialysis therapy, dehydration therapy, high-dose corticosteroid therapy, etc.

(2) Non-diabetic cerebrovascular accidents-low or high blood sugar, or mildly elevated stress blood sugar, but it is unlikely to be> 33.3mmol / L, and HbA1c is normal. Note: Cerebrovascular accident commonly used drugs often aggravate the disease, such as mannitol, hypertonic sugar, corticosteroids, etc. all increase the hypertonic state; phenytoin sodium can not inhibit the convulsions and seizures caused by hypertonic state, and can inhibit insulin secretion To further worsen hyperglycemia.

(3) Patients with a history of diabetes should also be distinguished from ketosis, lactic acidosis, and hypoglycemia.

(4) Acute pancreatitis-More than half of HNDC patients will have non-specific elevations in blood and urine amylase, and sometimes the increase is large. Note that acute pancreatitis cannot be diagnosed based on amylase elevation alone. However, it should be noted that some patients can indeed have acute pancreatitis at the same time, and even the onset of acute pancreatitis, so the changes of amylase need to be considered in conjunction with the clinical. Abdominal CT scans were performed on patients with abdominal pain and elevated amylase at the time of onset, and closely followed up. About 50% of patients in the early stage of acute pancreatitis have a temporary mild increase in blood glucose, but with the recovery of pancreatitis, most patients have reduced hyperglycemia within 2 to 6 weeks, while patients with acute hemorrhagic necrotizing pancreatitis have large pancreatic tissue Hemorrhagic necrosis, pancreatic islet cells are damaged, and the degree of damage is related to the severity and duration of the patient's glucose metabolism disorder. If the pancreatic islet cells are severely damaged, HNDC may be complicated.

First aid and treatment of acute complications of diabetes

The treatment principles of HNDC are the same as those of ketoacidosis, including actively finding and eliminating inducements, closely observing changes in the condition, and giving effective treatment to different people. Treatment methods include fluid replacement, use of insulin, correction of electrolyte disorders and acidosis.

(1) Rehydration quickly and massivelyAccording to the amount of water loss, the rehydration volume is calculated based on 10% -15% of body weight, the total amount is about 6-10L, 1/3 of the total amount should be entered within 4 hours, and the rest should be 12-24 After the infusion is completed within one hour, the fluid replacement rate and speed can be determined according to the central venous pressure, hematocrit, and average urine volume per minute. If shock has occurred before treatment, it is advisable to infuse normal saline and colloidal solution first to correct the shock as soon as possible. If there is no shock or shock has been corrected, after the infusion of normal saline, the plasma osmotic pressure is> 350mmol / L, and the blood sodium is> 155mmol / L. Consider infusion of a 0.45% sodium chloride hypotonic solution, and adjust the infusion under the monitoring of central venous pressure. Note speed. When the plasma osmotic pressure drops to 330mmol / L, the isotonic solution is reintroduced. Patients with heart disease should be reduced as appropriate.

(2) Insulin therapy-Patients are more sensitive to insulin. Continuous intravenous drip at a rate of 4-8u per hour makes the blood sugar drop slowly, and the blood sugar drops too quickly may cause brain edema. Due to insufficient blood volume and poor peripheral circulation, the effective concentration of islets in the blood cannot be stably maintained when subcutaneous injection of insulin, and after circulation is restored, a large amount of insulin enters the blood, which will cause hypoglycemia. Until the patient can enter the diabetic diet, change to subcutaneous insulin injection before the meal.

(3) Maintaining electrolyte balance-refer to the amount of urine in time to supplement potassium, that is, to be sufficient and prevent hyperkalemia. Monitor with blood potassium measurement and electrocardiogram. Pay special attention to those with renal dysfunction and oliguria.

(4) Acid-base balanceblood bicarbonate is lower than 9mmol / L. 5% sodium bicarbonate should be added. Check again after 4-6 hours. If bicarbonate is greater than 10mmol / L, stop adding alkali.

(5) Treatment of primary diseases, causes and complications-anti-infective treatment, stop all drugs that cause hypertonic state.

(6) dialysis treatment-suitable for the treatment of patients with HNDC and acute, chronic renal failure, diabetic nephropathy.

Prognosis of acute complications of diabetes

HNDC has a poor prognosis and a high mortality rate. Most literature reports 40% to 70% [6], especially when a large amount of hypotonic solution is used and blood glucose drops too quickly, it can easily cause cerebral edema. In addition, we must pay attention to the occurrence of pulmonary edema and heart failure. Most patients die from pre-existing or induced disease, and are related to factors such as age and pre-existing disease. The key to treatment is timely diagnosis and proper treatment. As the level of awareness of the disease continues to improve, the prognosis of HNDC will greatly improve.

Prevention of acute complications of diabetes

(1) Strengthen education and health checkups for diabetes knowledge, early detection and early treatment. Elderly people over 50 should regularly check blood sugar. Patients diagnosed with diabetes should take regular medication, control diet, strengthen exercise, and strictly control blood sugar levels.

(2) Control various inducing factors, actively treat various infections, and pay attention to whether there is dehydration when treating hemodialysis, peritoneal dialysis, and application of mannitol dehydration, and timely monitor blood glucose and urine sugar. Actively protect heart and kidney function.

(3) Pay attention to the application of induced drugs, such as diuretics, glucocortisol, propranolol (propranolol) and so on.

Nursing care for acute complications of diabetes

(1) Closely observe the changes in the condition, keep the breathing smooth, and prevent urinary tract and lung infections.

(2) Insulin pump care-When setting the pump, the needle of the insulin pump should be implanted in a place that does not hinder the movement, and care should be taken to avoid the site of trauma and scar. Generally put the pump in a bag or put it in a box and hang it on the waist to avoid being squeezed or dropped. After the pump is installed, you should always inspect it to avoid folding or blocking the tube. Pay attention to check the remaining amount of insulin in the pump and the puncture site of the needle. Prevent the needle from slipping out of the skin, routinely check the infusion site daily, and observe whether there is redness, swelling and bleeding. If the above symptoms occur, the infusion site should be replaced in time. Familiar with common causes of insulin pump alarms and be able to deal with them in a timely manner. Accurate control of insulin dosage and speed is essential for treatment. Blood glucose monitoring is performed every 1 to 2 hours with a blood glucose meter, and the insulin infusion speed is adjusted in time according to the blood glucose to ensure smooth and stable hypoglycemia. At the same time pay attention to hypoglycemia response, find changes in the situation in a timely manner.

(3) Basic nursingBecause the patient is lying in a coma and has poor skin resistance, the sheets should be kept clean, dry and flat, massage the pressured part, promote blood circulation, and prevent pressure ulcers. For patients with pulmonary infections, you should step back and pat your back to promote sputum excretion and suction if necessary; for patients with urinary tract infections, you should keep the ureter and perineum clean. Patients with dysphagia of the cerebral infarction should prevent aspiration pneumonia by mistake when eating. Careful oral, skin, perineal, and eye care, keep the airway open, provide appropriate care for the patient's primary disease, and provide the patient with a neat, quiet, comfortable and safe hospital environment.

(4) Psychological nursing and health educationIntroduce the purpose, precautions, and understanding support and cooperation of the patient's family to the patient's family. With the patient's condition stable, his mind cleared, blood glucose control, and timely psychological care to help the patient Correctly establish the confidence to overcome the disease, explain to them the knowledge of diabetes and the prevention of various complications, and eliminate their nervousness and fear, so as to obtain close cooperation between patients and their families in the implementation of various treatment and nursing operations. Because most patients are old and have poor physical foundations, they help family members of diabetics understand the knowledge of diabetes and care to help patients give them spiritual support and life care. With the widespread use of insulin, it is not enough just to let patients know the brand name and appearance of the drug. It is necessary to let patients know the type of insulin they use, the time of use and the peak time of the effect of the drug, so that patients can manage their blood glucose more effectively. Through education, patients know that eating insulin on time after injection and carrying biscuits and sweets when going out can improve the importance of diabetes patients on the response to hypoglycemia.

(5) Guidance for dischargeemphasize to patients and their families that factors that may induce NHDC should be avoided, reasonable diet and correct injection of insulin as required, maintain a good mood, develop good health habits, and actively control diabetes to avoid complications.

(6) PrecautionsThe key to nursing is to closely observe changes in the condition, monitor vital signs, quickly rehydrate and use insulin properly, strengthen basic care, master diabetes expertise and operation skills, implement psychological nursing and health education, and strengthen the relationship with patients Communicate with family members to improve patient self-management and family care ability. ^[4]

Acute complications of diabetes lactic acidosis

Causes of acute complications of diabetes

(1) Excessive production of lactic acid-chronic complications of diabetes, such as combined heart, lung, liver, and kidney disease, resulting in hypoxia in tissues and organs, resulting in increased lactic acid production; diabetes patients with impaired glucose metabolism, elevated levels of glycated hemoglobin, and hemoglobin Decreased oxygen carrying capacity, resulting in local hypoxia, resulting in increased oxidation of pyruvate and increased lactic acid production; peripheral circulatory failure during shock, tissue ischemia and hypoxia, increased lactic acid production; alcohol abuse causes acute ethanol poisoning, alcohol in ethanol dehydrogenase Under the action of acetaldehyde, acetaldehyde is oxidized to produce acetic acid, and further metabolism of acetic acid causes the body to increase lactic acid; carbon monoxide poisoning can directly inhibit the role of cytochrome oxidase in the respiratory chain, reduce the oxygen content of arteries, and cause hypoxemia. Lactic acid poisoning; Catecholamines can contract skeletal muscles and intrahepatic blood vessels, causing liver lactic acid function to decline, muscles release lactic acid due to tissue hypoxia, and increase blood lactic acid.

(2) Inadequate clearance of lactic acid-acute complications of diabetes, such as infection and ketoacidosis, can cause lactic acid accumulation and induce LA; chronic complications of diabetes, such as liver and kidney dysfunction, can affect the metabolism, transformation and Excretion; Biguanide antidiabetic drugs are used improperly (excessive dose or improper selection), especially phenformin, which has a long half-life and slow excretion, can inhibit liver and muscle tissues from taking up lactic acid; inhibits the conversion of lactate to glucose in mitochondria, causing lactic acid Accumulation; large doses or long-term use of acetaminophen can cause fulminant liver necrosis and impede lactic acid clearance.

The pathogenesis of acute complications of diabetes

LA is a type of diabetic metabolic complication caused by the blockage of glucose oxygenation in diabetic patients, an increase in glucose hydrolysis, and the production of a large amount of lactic acid, which makes lactic acid synthesis greater than degradation and excretion of lactic acid in the body. Lactic acid is the end product of anaerobic fermentation of glucose and is reduced by pyruvate. The breakdown of glucose is divided into aerobic oxidation and anaerobic fermentation. Aerobic oxidation refers to the main way that energy is produced by the breakdown of sugars in the body. Under anaerobic conditions, glucose is hydrolyzed in the cytosol. The intermediate product pyruvate is converted to lactic acid by hydrogenation of reduced coenzyme I (NADH) under the action of lactate dehydrogenase, and NADH is converted to coenzyme I ( NAD +). Lactic acid can also be oxidized to pyruvate when NAD + is converted to NADH under the action of lactic dehydrogenase. This is a reversible reaction catalyzed by lactic dehydrogenase. Pyruvate can enter the mitochondria for further oxidation under aerobic conditions. Under the catalysis of pyruvate carboxylase, acetyl-CoA is formed, which is then decomposed into H2O and CO2 by tricarboxylic acid cycle oxidation capacity. In addition, pyruvate can also be metabolized to glucose via pyruvate carboxylation. When mitochondria are dysfunctional due to relative or absolute hypoxia of the tissue, pyruvate easily accumulates in the cytoplasm and turns into lactic acid, which gradually accumulates, and LA occurs. The main parts of lactic acid production in the body are skeletal muscle, brain, red blood cells and skin; the main parts of metabolic clearance are liver and kidney. Under normal circumstances, lactic acid produced during the body's metabolism is mainly oxidized in the liver, or is converted into glycogen storage, and a small amount of lactic acid is excreted by the kidneys. Therefore, insufficient lactic acid clearance is more common in liver diseases, with cirrhosis being the most common.

Clinical classification of acute complications of diabetes

LA is clinically divided into two categories, congenital and acquired.

(1) Congenital LAInfants with LA without shock are mostly congenital metabolic abnormalities, mostly due to genetic enzyme defects causing lactic acid and pyruvate metabolism disorders, such as lack of glucose-6-phosphatase and pyruvate carboxylase. , Fructose-1, 6-bisphosphatase, pyruvate dehydrogenase.

(2) Acquired LA Most LAs are acquired. According to the results of the Cohen and Woods classification revisions, acquired LAs can be divided into two types: A and B. Type A is secondary LA and is more common than type B. It is seen in a variety of shocks with hypoxia, such as dehydration, hemorrhagic (hypovolemic) shock, septic shock (severe sepsis), anaphylactic shock, asthma When the persistent state is accompanied by congestion and hypoxia in the surrounding tissues, the pathogenesis is that the oxygen obtained by the tissues cannot meet the metabolic needs of the tissues, leading to an increase in anaerobic fermentation and the production of type A LA. Type B is spontaneous LA, which is seen in many non-shock states, and its pathogenesis is not related to tissue hypoxia. It can be further divided into 3 subtypes. Type B1 is related to common diseases such as diabetes, sepsis, liver and kidney failure, diabetes, malignant tumors, malaria, and typhoid fever, and type B2 is related to drugs or poisons, such as biguanides, water Salicylic acid, methanol, ethylene glycol, cyanide, nitroprusside, niacin, catecholamine, diethyl ether, papaverine, paracetamol, nalidixic acid, isoniazid, streptozotocin, sorbitol, lactose, tea Alkali, cocaine, paraldehyde and ethanol. Type B3 is associated with other factors such as strenuous muscle activity and seizures.

Pathophysiology of acute complications of diabetes

(1) Biguanides and LA-many drugs can cause LA, the most common of which are biguanides (phenformin and metformin), especially phenformin, which has been used to treat diabetes since the 1950s. Often induced lethal LA has been discontinued in many countries. Phenformin is known to promote the utilization of glucose in peripheral tissues and the conversion of glucose to lactic acid. Practice has shown that the use of phenformin can increase the production of lactic acid and reduce the uptake of the liver. Phenformin can inhibit ATP synthesis, the ATP / ADP ratio decreases, and oxidative phosphorylation and glycogenogenesis are inhibited, so lactic acid oxidation is reduced and production is increased. Although phenformin causes a moderate increase in blood lactic acid levels, most of the LAs associated with phenformin are either due to excessive doses or are associated with diseases such as severe liver and kidney failure, heart failure, and shock. Metformin is another biguanide, and its chance of causing LA is significantly less than that of phenformin (about 1/50 of it). Metformin is widely used at home and abroad now. It may be because metformin is water-soluble and it is not easy to accumulate in the body. When it lowers blood sugar, the effect of increasing lactic acid production in peripheral tissues is not obvious. The treatment dose generally does not cause LA.

(2) Diabetes and LA-Type 2 diabetes may have mild hyperlactic acid in the basic state, which may be mainly related to oxidative defects of lactic acid. In addition, absolute or relative lack of insulin can reduce mitochondrial pyruvate utilization, increase glycolysis, and increase lactic acid production. In ketoacidosis, the blood lactic acid concentration may increase several times and exacerbate metabolic acidosis. At this time, hyperlactic acidemia may be partly due to ketone body inhibition of liver uptake and decreased circulating blood volume, which results in insufficient tissue perfusion. Hypertonic non-ketogenic coma is more likely to cause severe LA than ketoacidosis. Hypertonic non-ketogenic coma is more common in the elderly, and the risk of secondary liver and kidney and cardiopulmonary insufficiency is further increased.

(3) Septic shock and LA-When septic shock occurs, endotoxin and other bacterial products initiate a series of metabolic reactions that lead to the synthesis and release of inflammatory mediators, cytokines and vasoactive substances in the body, impairing vasomotor tension and increasing microvessels. Permeability, promote the accumulation of white blood cells and platelets. The leakage of fluid from capillaries reduces the effective circulating blood volume and cardiac output (circulating bacterial products can also directly damage left ventricular function). Eventually, the above-mentioned changes caused a decrease in systemic blood pressure, followed by increased adrenal and sympathetic nerve activity leading to vasoconstriction and decreased blood flow to the skin and internal organs (including liver and kidneys). The aforementioned metabolic and hemodynamic factors lead to increased production of lactic acid. Decreased hepatic portal blood flow also limits the liver's uptake of lactic acid. Tissue hypoperfusion reduces oxygen supply, leading to impaired respiratory chain function and oxidative phosphorylation. Insufficient mitochondrial synthesis of ATP does not effectively oxidize NADH and consume protons. Decreased ATP levels in the cytoplasm stimulate PFK activity and increased glycolytic rate. ATP deficiency and systemic pH decline also inhibit liver and kidney energy-consuming glycogenogenesis, further inhibiting tissues' ability to clear lactic acid.

(4) Cancer and LAIn cancer, malignant tumor cells generally have an inherently enhanced anaerobic glycolytic activity, so that when tumor cells are present in large numbers, overall lactic acid production increases. LA associated with most cancers is found in hematological malignancies, or extensive liver infiltration of tumors. LA in cancer patients is mostly due to increased lactic acid production in tumor cells, accompanied by liver and kidney dysfunction or sepsis, which impairs the uptake and utilization of lactic acid and protons.

(5) Total parenteral nutrition and LA-parenteral nutrition may induce LA, even in the absence of related diseases. Ingredients for total parenteral nutrition include carbohydrates in addition to glucose, as well as fructose or sorbitol (which can be metabolized to fructose). Metabolic acidosis may be a direct result of the aforementioned sugar metabolism. Fructose is phosphorylated in the cell to fructose 1-phosphate, which is subsequently converted to glyceraldehyde and dihydroxyacetone phosphate. One molecule of fructose is consumed by the metabolism of the three-carbon intermediate to consume two molecules of ATP. In the liver, reduced levels of high-energy phosphate bonds inhibit glycogenogenesis and stimulate glycolysis, which may lead to LA in individuals with metabolically compensated states.

(6) Acute ethanol poisoning and LA-ethanol is mainly oxidized to acetaldehyde in cells under the catalysis of alcohol dehydrogenase, and acetaldehyde is further oxidized to acetic acid under the catalysis of aldehyde dehydrogenase. , Increase the intracellular NADH / NAD + ratio, which is conducive to the conversion of pyruvate to lactic acid; In addition, ethanol can still inhibit pyruvate gluconeogenesis, chronic chronic alcoholism can cause vitamin deficiency and liver damage, and can also reduce pyruvate Oxidation and gluconeogenesis. Therefore, alcoholism can lead to LA by directly increasing lactic acid production and indirectly inhibiting lactic acid clearance.

Clinical manifestations of acute complications of diabetes

(1) Multiple groups

This disease is mainly seen in elderly patients with diabetes and chronic heart and lung disease or liver and kidney dysfunction taking biguanide drugs. Once infection, dehydration, decreased blood volume, hunger, etc., LA is easily induced.

(2) Symptoms of the disease

LA is more acute and mild: only fatigue, nausea, vomiting, decreased appetite, abdominal pain, dizziness, drowsiness, lethargy, and deep breathing. Moderate to severe: May have nausea, vomiting, headache, dizziness, tenderness of the whole body, cyanosis of lips, deep breathing (without ketone odor), decreased blood pressure and temperature, weak pulse, fast heart rate, dehydration, and disturbance of consciousness , Drowsiness, stiffness, lethargy and other symptoms, more severe cases can cause coma. Hypoxia caused by cyanosis, shock and primary symptoms. Drug-induced people often have a history of taking medication and corresponding manifestations of poisoning. However, the symptoms and signs of the disease may not be specific, and the mild clinical manifestations may not be obvious. They are often covered by the symptoms of the primary or induced disease. Care should be taken to avoid misdiagnosis or missed diagnosis.

(3) Disease hazard

Severe acidosis can cause damage to multiple organs in the body and needs to be corrected as soon as possible. And the mortality rate of LA is higher, and it increases with the increase of blood lactic acid level. It has been reported in the literature that the mortality rate is 20% when the blood lactate is 1.4 to 4.4 mmol / L, the mortality rate is increased to 74% when the blood lactate is 4.5 to 8.9 mmol / L, and the mortality rate is 90% when the blood lactate reaches 9.0 to 13 mmol / L. When blood lactic acid was> 13mmol / L, the mortality was as high as 98%.

Diagnosis and diagnosis of acute complications of diabetes

I. Diagnosis

(1) Medical history: Patients with diabetes have an excess of biguanide drugs (more than 75mg / d of metformin and metformin of more than 2000mg / d), and their condition worsens; patients with diabetes have liver and kidney insufficiency, hypoxia or surgery, etc. ; Diabetes patients with multiple causes of shock, and metabolic acidosis without significant increase in ketone body, should be highly suspected of this disease.

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Prognosis of acute complications of diabetes

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Pathophysiology of acute complications of diabetes

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The central nervous system is most sensitive to hypoglycemia. Because nerve cells themselves have no reserves, their energy requirements are almost entirely dependent on blood glucose supply, even in type 1 diabetes. This is because glucose is not needed by brain cells for peripheral insulin. The central nerve consumes about 6g of glucose per hour. The source of brain cell energy decreases during hypoglycemia, and neurological symptoms or neuroglycopenia soon appear. Initially manifested as mild impairment of mental and mental activity, followed by symptoms of inhibition of the cerebral cortex, followed by successive involvement of the subcortical center and the brainstem. Eventually, the medulla oblongata is involved and changes in respiratory circulation are caused. Death often occurs if hypoglycemia cannot be reversed. It is suggested that the order of central nervous system damage is related to the development and evolution of the brain. The more the cells evolve, the more sensitive they are to hypoglycemia. When glucose is replenished, the central nervous system recovers in the reverse order.

In addition to directly affecting the function of the central nervous system, hypoglycemia also affects the functional activities of the sympathetic chromaffin system through the central nervous system, causing a series of symptoms of sympathetic nerve excitement, such as palpitations, tremors, paleness, and sweating. This group of symptoms is mediated by the stimulation of 2 adrenergic receptors. Patients with undetected hypoglycemia often have abnormal 2 adrenergic signaling pathways.

Clinical manifestations of acute complications of diabetes

The symptoms of diabetic hypoglycemia vary, and most feel weak and difficult to support. Symptoms of sympathetic nerves and central nervous system symptoms usually appear.

Sympathetic nerve excitement symptoms: mainly shaking hands, cold sweats, palpitations, hunger, and restlessness. However, when diabetes is complicated by autonomic dysfunction, these manifestations are not obvious or relatively slow.

Central Nervous Symptoms: Mainly headache, dizziness, blurred vision, sometimes disorientation, lack of desire, lethargy, and in severe cases, coma or seizures

The occurrence of hypoglycemia is very insidious and sometimes begins to be difficult to detect. Fragile diabetic patients are prone to sudden onset, and most of them are acute. The clinical manifestations of senile hypoglycemia are often not typical and should be examined carefully to find out.

Diagnosis and diagnosis of acute complications of diabetes

Laboratory inspection

(1) The blood glucose is lower than the normal lower limit, and <2.8mmol / L can diagnose hypoglycemia.

(2) A glycated hemoglobin test> 7% may indicate an acute episode of hypoglycemia; <7% may have a chronic hypoglycemia after a long period of time.

(3) Examination of ketones in blood and urine. Increased ketones in the blood. Positive ketones in the urine indicate enhanced fat catabolism and starvation ketosis.

Differential diagnosis of acute complications of diabetes

The diagnosis is mainly based on the blood glucose concentration at the time of the onset of the symptoms. When the blood glucose is> 4.0mmol / L, the diagnosis can be ruled out. If <2.5mmol / L is recurring, the diagnosis can be basically confirmed. The standard can be set to <3.0mmol / L.

This disease should be diagnosed with epilepsy, syncope, brain tumor, cerebrovascular accident, painless myocardial infarction, snoring and other causes of coma.

Treatment of acute complications of diabetes

First, emergency treatment

1. Self-rescue Once the patient confirms the symptoms of hypoglycemia, they should immediately eat food containing 20-30g sugars or oral sugar water, instead of having to take blood glucose tests at each episode. Excessive eating can cause hyperglycemia after the episode. When you can not confirm hypoglycemia, you should do a quick blood glucose test yourself, or go to the nearby hospital for emergency treatment. If the patient has severe hypoglycemia and cannot help themselves, relatives and friends should help take sugar or sugar-rich foods, and those who have swallowing function and have glucagon can inject 1mg of glucagon. If self-rescue fails to improve, or if hypoglycemia has severe confusion, convulsions, chest pain, hypotension and other symptoms, they should be sent to the hospital for emergency treatment.

2. Rescue in the hospital All patients with suspected hypoglycemia should be replenished with glucose immediately after taking samples and / or rapid blood glucose measurement. If the symptoms of hypoglycemia are quickly relieved or the consciousness of the coma is clear, it is a strong evidence of hypoglycemia. Usually 40% intravenously with 50% glucose. In order to prevent recurrence of hypoglycemia, intravenous drip of 10% glucose solution should be continued for maintenance. Hypoglycemia caused by chlorpromide or glibenclamide, sugar supplementation lasts at least 2-3 days. Those with difficulty in intravenous injection should immediately inject intramuscularly or subcutaneously 1 mg of glucagon (15 g, kg for children), and then try to establish a venous pathway. Usually, the blood glucose concentration rises 10-15 min after glucagon injection, and the glycemic effect continues for about 1 -2h.

Second, remission treatment

After the correction of hypoglycemia, various possible complications should be treated in time. Adjust insulin or oral hypoglycemic dose. Eliminate incentives to prevent recurrence of hypoglycemia.

Prognosis of acute complications of diabetes

(1) Early detection and timely treatment of hypoglycemia of diabetes, generally good prognosis.

(2) Most patients with moderate hypoglycemic coma can recover after timely rescue treatment, and the prognosis is still good.

(3) Severe hypoglycemic coma, after a long period of time, although rescue treatment, but serious damage to brain cells, it is difficult to reverse, with adverse sequelae, such as memory loss, slow response and even dementia.

(4) Hypoglycemic coma occurs severely in type 1 diabetes, with a poor prognosis and a mortality rate of 0.4%.

(5) A small number of elderly patients with diabetes and hypoglycemia are prone to diabetic heart disease, arrhythmia, myocardial infarction and other poor prognosis.

Prevention of acute complications of diabetes

(1) Extensive publicity and education should be carried out to enable diabetic patients and their families to understand the causes and symptoms of hypoglycemia. Mild hypoglycemia should be handled in time to prevent hypoglycemia from mild to hypoglycemic coma.

(2) Diabetics should regularly check blood sugar and urine sugar, and work closely with physicians when they have a tendency to hypoglycemia to determine the cause of hypoglycemia, or take oral sugar water or follow a doctor's treatment in time.

(3) Inject insulin or oral hypoglycemic drugs to avoid large doses or increase the dose by yourself to prevent hypoglycemia.

(4) Meals should be taken after the insulin injection, and refusing to eat or fasting after the insulin injection is forbidden.

(5) The diet structure should be reasonable to prevent partial food from eating only protein and fat. This is a wrong diet method and should be avoided.

(6) Islet -cell tumors are often excluded before fasting hypoglycemia occurs before breakfast. ^[7]