Diabetic ketoacidosis

Introduction to diabetic ketoacidosis Diabetic ketoacidosis refers to the obvious deficiency of insulin in the diabetic patients under various incentives, the abnormal growth of raw sugar hormones, high blood sugar, high blood ketone, ketonuria, dehydration, electrolyte imbalance, metabolic acidosis, etc. Symptoms of pathological changes are one of the common emergencies in internal medicine. Ketoacidosis can be divided into mild, moderate and severe according to its degree. Mildness refers to simple ketosis and no acidosis; mild to moderate acidosis can be classified as moderate; Severe refers to ketoacidosis accompanied by coma, or although there is no coma, but the carbon dioxide binding force is less than 10mmol / L, the latter is easy to enter a coma. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: cerebral edema hypoglycemia adult respiratory distress syndrome pulmonary edema arrhythmia myocardial infarction shock sudden death cerebral thrombosis pulmonary embolism acute renal failure sepsis diffuse intravascular coagulation lactic acidosis acute pancreatitis acute gastric dilatation

Causes of diabetic ketoacidosis

Acute infection (30%):

It is an important cause of DKA, including the respiratory system, urinary system and skin infections, and the incidence is high in winter and spring. Acute infection is a complication of DKA. It is a cause and effect with DKA, forming a vicious circle and increasing the complexity of diagnosis and treatment. Sex.

Improper treatment (25%):

Such as discontinuation of drugs (especially insulin) treatment, insufficient drug and drug resistance, especially in patients with type 1 diabetes, discontinuation or reduction of insulin treatment dose, often cause DKA, type 2 diabetes patients take large amounts of phenformin for a long time, especially DKA is easily induced in liver and kidney function; large doses of thiazide diuretics have also been reported. In recent years, some patients have convinced that there is no definitive therapeutic treatment or "drug", and they have given up scientifically recognized formal treatment. In particular, patients with type 1 diabetes, even with insulin discontinuation, are more likely to induce DKA.

Improper diet (20%):

Out of control of the diet and/or gastrointestinal diseases such as overeating, too sweet (too much sugar) or deficiency, alcoholism, or vomiting, diarrhea, etc., can aggravate metabolic disorders and induce DKA.

Other factors (20%):

Such as severe trauma, anesthesia, surgery, pregnancy, childbirth, mental stimulation, and myocardial infarction or cerebrovascular accidents, elevated levels of glucocorticoids due to stress, increased sympathetic nervous system excitability, and eating disorders, Easy to induce ketoacidosis.

Pathogenesis

The basic link in the pathogenesis of DKA is due to insulin deficiency (Figure 1) and insulin counter-regulating hormone (such as glycemic hormone), leading to glucose metabolism disorders, blood glucose can not be used normally, resulting in increased blood sugar, increased fat decomposition, increased blood ketones and secondary A series of changes in metabolic acidosis and water, electrolyte imbalance, etc., glycosaminoglycans include glucagon, adrenaline, glucocorticoids and growth hormone, of which glucagon has the strongest effect, glucagon secretion Too much is the main cause of the onset of DKA. Due to the double barrier of insulin and glycemic hormone secretion, the function of glucose running carrier is reduced, the glycogen synthesis and sugar utilization rate are decreased, glycogen decomposition and gluconeogenesis are enhanced, and blood sugar is significantly increased. At the same time, due to the disorder of fat metabolism, the level of free fatty acids increased, providing a large number of precursors for the production of ketone bodies, eventually forming ketoacidosis.

In DKA, the pathophysiological changes that occur in the body are mainly reflected in the following aspects:

1. Hyperglycemia: DKA patients have a moderate increase in blood glucose, usually 300 ~ 500mg / dl, unless the renal insufficiency, or more than 500mg / dl, causing high blood sugar in patients including insulin secretion Decreased, the body's response to insulin decreased, the secretion of glycemic hormone increased, as well as dehydration, blood concentration and other factors.

The effects of hyperglycemia on the body include: 1 affecting the extracellular fluid permeation zone. Generally, the osmolality of 5.6mmol/L (100mg/dl) increases by 5.5mmol/L (5.5mOsm/kg), extracellular fluid. Hypertonicity causes intracellular fluid to move outside the cell, dehydration of the cell, and dehydration of the cell will lead to dysfunction of the corresponding organ, 2 causing osmotic diuresis, and increased blood glucose by DKA can be compared with normal 5.5 to 11.1 mmol/ (L·min) is 5 to 10 times higher, and the maximum capacity of the proximal tubule to recover sugar is 16.7 to 27.8 mmol/(L·min). Excess sugar is excreted by the kidneys, taking away moisture and electrolytes, further causing Water and salt metabolism disorders.

2. Ketoacidosis and/or acidosis

(1) Composition and metabolism of ketone bodies: ketone bodies are products of incomplete oxidation of fat , including acetoacetic acid, -hydroxybutyric acid and acetone. Among them, acetoacetic acid is a strong organic acid, which can be combined with ketone body powder. The color reaction occurs; -hydroxybutyric acid is a reduction product of acetoacetic acid, which is also a strong organic acid, which is the largest in the ketone body, accounting for 70% of the total amount of the ketone body; acetone is the decarboxylation product of acetoacetate, the amount is the least. Neutral, no renal threshold, can be discharged from the respiratory tract, normal human blood ketone body does not exceed 10mg / dl, ketoacidosis can be increased 50 to 100 times, urinary ketone positive.

It can be seen from Fig. 3 that the acetylated CoA, a product of fatty acid oxidation, is both a precursor of the ketone body and an inevitable pathway for the elimination of the ketone body. The acetyl CoA is combined with the oxaloacetate, a product of sugar metabolism, to form citric acid, and then enters the tricarboxylic acid. If it is recycled, if there is not enough sugar metabolite oxaloacetate, the elimination of the ketone body is an obstacle.

(2) Increased lipolysis: The main causes of fatty acid breakdown in DKA patients include severe insulin deficiency, inhibition of fat breakdown, sugar utilization disorders, increased compensatory fat mobilization, and growth hormone, glucagon and cortisol in DKA. Caused by factors such as increased hormone breakdown of fat.

(3) Hyperketolemia: DKA patients have increased fat decomposition, producing a large amount of free fatty acids and triglycerides. A large number of free fatty acids are -oxidized in the liver and coupled with CoA and ATP to form acetyl CoA. CoA increases the ketone body produced in the liver, which exceeds the ability of normal surrounding tissues to oxidize and causes hyperketosis.

(4) Acidemia and ketoacidosis: Both -hydroxybutyrate and acetoacetate in the ketone body are strong acids, and the increase in blood ketone increases the concentration of organic acids in the blood (normal 6mmol/L), while a large amount of organic acids When excreted from the kidney, except for a small amount of free state or by the renal tubular secretion [H] neutralization and elimination, most of the bases are combined with the body to form a salt and eliminated, resulting in a large loss of alkali storage in the body and acidosis, when blood Typical acidosis breathing (Kussmaul respiration) can occur when the pH drops to 7.2. When pH <7.0, it can cause central paralysis or severe muscle weakness or even death. In addition, acidemia affects the oxygenation of hemoglobin from tissue, resulting in hypoxia. Aggravate the deterioration of the general condition.

The degree of perception of DKA varies widely, regardless of whether the state of consciousness is semi-awake or coma. When plasma HCO-3 9.0mmol/L, it is considered to be regarded as diabetic ketoacidosis and coma. , DKAC), when the blood HCO-3 drops below 5.0mmol / L, the prognosis is extremely serious.

3. Dehydration: DKA has a significant increase in blood sugar, and a large number of acid roots, osmotic diuresis and acid loss, plus deep breathing loss and possible vomiting, diarrhea caused by diarrhea and other factors, It can lead to the occurrence of dehydration. The causes of dehydration are: 1 osmotic diuresis caused by hyperglycemia; 2 protein and fat decomposition increase, a large amount of acidic metabolites are taken away when water is removed; 3 patients have insufficient water intake, especially in elderly patients, caused by dehydration Insufficient blood volume, decreased blood pressure and even circulatory failure.

4. Electrolyte disorder: DKA, due to osmotic diuresis, reduced intake and vomiting, transfer of water inside and outside the cell into the blood, blood concentration, etc. can lead to electrolyte imbalance, clinically measured blood electrolyte levels can be high, can be low, also It can be normal. There is no fixed change of blood Na in DKA. It is generally normal or reduced. In the early stage, the intracellular fluid can cause dilute low Na. In general, the blood sugar can increase by 5.6mmol/L, and the blood Na can decrease by 2.7mmol/L. Loss of blood Na may increase due to diuretic and ketone excretion, but if the water loss exceeds Na, the blood Na may increase, and the blood K may decrease, although the tissue decomposition is increased by DKA and a large amount of intracellular K is removed. The blood K value is not low, but its overall potassium is still low, because: 1 osmotic diuresis causes a large amount of K loss; 2DKA when renal tubular secretion [H] and system [NH4] function is impaired, renal tubular Na-K exchange Increase; 3 vomiting and insufficient intake, therefore, as long as the renal function is not impaired in DKA patients, potassium is required for treatment.

In DKA, due to the increase of cell catabolism, the loss of phosphorus also increases, and hypophosphatemia can occur clinically. In recent years, special attention has been paid to the decomposing of DKA patients due to increased cell decomposition, the organic binding of phosphorus in cells will be destroyed, and phosphorus is released from cells. Urinary discharge, about 11% of DKA patients with low blood phosphorus, phosphorus deficiency can cause red blood cell 2,3-diphosphoglycerol reduction, and affect oxygen from hemoglobin dissociation caused by tissue hypoxia.

In addition, it should also be noted that DKA may cause a false decrease in water-soluble electrolyte components (such as blood sodium) due to increased blood lipid levels.

5. Tissue hypoxia: DKA with abnormal oxygen system, hyperglycemia causes increased glycosylated hemoglobin (GHb) content in red blood cells, enhances the affinity of hemoglobin and oxygen; intracellular 2,3-diphosphoglycerate in the absence of phosphorus (2,3 -DPG) reduces, the blood oxygen dissociation curve shifts to the left, both of which lead to a decrease in oxygen release, resulting in tissue hypoxia, but due to the Bohr effect, that is, the pH value decreases during acidosis, the hemoglobin and oxygen affinity decrease, but also The tissue hypoxia is improved to some extent.

Diabetic ketoacidosis prevention

DKA can be prevented. In the treatment of diabetes, publicity and education on diabetes knowledge should be strengthened, and prevention should be emphasized. Especially for type 1 diabetes, strict insulin therapy system should be emphasized, insulin therapy should not be interrupted or insulin dose reduced, and insulin should be Must pay attention to proper preservation (2 ~ 8 ° C), especially in the summer high temperature season, in order to avoid failure, patients with type 2 diabetes should be alert at all times to prevent various causes, especially infection and stress, whether it is type 1 or type 2 Diabetes, even during illness, such as fever, anorexia, nausea, vomiting, etc., can not stop or interrupt insulin therapy due to less eating, diabetes with mild infection, extra-hospital treatment, should pay attention to monitoring blood sugar, blood ketone or ketone body; In the case of myocardial infarction, surgical acute abdomen surgery and severe infection, insulin should be given in time. Patients with severe type 2 diabetes who have failed oral hypoglycemic drugs should be switched to insulin therapy in time to prevent ketosis. In short, DKA can prevent it. Prevention of DKA is more effective and important than rescuing the already affected.

Diabetic ketoacidosis complications Complications cerebral edema hypoglycemia adult respiratory distress syndrome pulmonary edema arrhythmia myocardial infarction shock dying cerebral thrombosis pulmonary embolism acute renal failure septic diffuse intravascular coagulation lactic acidosis acute pancreatitis acute gastric dilatation

Complications that may occur during the treatment of ketoacidosis.

Brain edema

It has been reported that symptomatic or even fatal brain edema can occur during DKA treatment. It is more common in adolescents. Symptomatic cerebral edema is rare in adults, but clinical studies have reported that EEG and CT are often used within the first 24 hours of DKA treatment. It shows the occurrence of subclinical cerebral edema, mostly due to blood sugar, blood sodium drops too fast, blood osmotic pressure drops rapidly, water enters brain cells and brain interstitial; in addition, if acidosis is corrected too fast, oxygen separation curve Left shift, central nervous system hypoxia, aggravation of cerebral edema, abnormal cerebrospinal fluid acidosis is also associated with cerebral edema, its clinical manifestations are often treated, after the patient's consciousness once turned clear, and then coma, and often accompanied by jet vomiting, Need to be vigilant, once the diagnosis is confirmed should be actively rescued, to reduce the intracranial pressure treatment.

2. Hypokalemia

The current low-dose insulin therapy, the slower liquid infusion rate and the improvement of the treatment method of careful supplementation of alkali, reduce the rate of extracellular potassium transfer to the cells, and reduce the occurrence of iatrogenic hypokalemia, but it should be noted With the replacement of saline, insulin, glucose and acidosis, all of them can reduce blood potassium. As long as DKA patients are treated with the above treatment and have urination, blood potassium and potassium supplement should be continuously monitored. For each infusion of liquid 1L, blood potassium is measured once. If the amount of insulin is >0.1U/(kg·h), the interval between blood potassium monitoring should be shorter.

3. Low blood sugar

When DKA is treated, the blood sugar returns to normal and is usually faster than the correction of ketoacidosis. At this time, if insulin is continuously administered without infusion of glucose, hypoglycemia will occur, and blood glucose should be measured once every 1 hour after the start of treatment. 4 times; then every 1 hour, once every 4 hours; once every 4 hours, generally require blood glucose to drop at a rate of 3.33 to 5.56 mmol / L per hour, once the blood glucose reaches 13.9 ~ 16.7 mmol / L, insulin The input speed is halved and 5% or 10% glucose fluid is added to avoid hypoglycemia.

4. Hyperchloremia

Hyperchloremia or hyperchloric acidosis often occurs in the recovery process of DKA treatment: when 1DKA, the loss of Cl- is less than the loss of sodium, and the supplemented saline contains the same amount of Na and Cl-, which can cause relative hyperchloremia. In the recovery of 2DKA, Na and HCO3- are transferred to the cells, while Cl- is excessively left outside the cell; during the recovery period of 3DKA, the ketone anion is metabolized to produce NaHCO3, which leads to hyperchloric acidosis, and if an anion is treated during DKA treatment The gap is gradually normal, and subsequent high-chlorine non-anionic interstitial acidosis is generally not clinically significant.

5. Adult respiratory distress syndrome (ARDS)

Very rare, but may be a potential, fatal complication during DKA treatment. In patients with DKA, the arterial oxygen partial pressure (PaO2) and alveolar-arterial oxygen gradient (A-aO2) are normal, at this time, due to the obvious in vivo Dehydration and NaCl deficiency, the body colloid osmotic pressure increased, with the hydration treatment and electrolyte supplement, the colloid osmotic pressure decreased progressively, so that it was significantly lower than normal, with the decrease of colloid osmotic pressure, PaO2 reduction and A-aO2 gradient Increased, this is clinically significant in most patients, does not cause clinical signs and symptoms, chest X-ray is normal, only a small number of patients progress to ARDS during treatment, rapid input of crystal, increase left atrial pressure and reduce plasma colloid Osmotic pressure, the above changes can cause the formation of pulmonary edema, even in the case of normal heart function, the appearance of lung snoring and the widening of A-aO2 gradient suggesting the risk of ARDS during DKA treatment, the fluid loss should be reduced for these patients. Note the speed, especially in the elderly or patients with a history of heart disease, regular monitoring of blood gas analysis and A-aO2 gradient can help prevent the occurrence of ARDS.

6. Infection

It is also one of the common complications of DKA. It is often easy to develop infection due to the decrease of anti-infective resistance of the body. It is also easy to use certain broad-spectrum antibiotics to cause pathogenic bacteria to grow and cause fungal infection.

8. Cardiovascular system:

When the fluid is too fast, it can lead to heart failure; when potassium or high potassium is lost, arrhythmia or even cardiac arrest is easy to occur; when the blood sugar is lowered too fast or the blood sugar is too low, myocardial infarction may occur, or even shock or sudden death When the blood is concentrated and the blood coagulation factor is strengthened, it may cause complications such as cerebral thrombosis and pulmonary embolism.

9. Acute renal failure:

Most of them are complicated by the dehydration, shock, and severe decline of the renal circulation.

11. Severe infection and sepsis:

It often worsens the condition, is difficult to control, and affects the prognosis.

12. Diffuse intravascular coagulation (DIC):

Due to serious infections such as sepsis and shock, acidosis, etc., the disease is complicated.

13. Diabetic hyperosmolar coma and lactic acidosis:

Among the diabetic ketoacids, the poison may be associated with this syndrome.

14. Other:

Such as acute pancreatitis, acute gastric dilatation and so on.

Symptoms of diabetic ketoacidosis Common symptoms Abdominal pain Gastrointestinal symptoms Breathing sweet smelly fainting Nausea coma Loss of appetite Dizziness Cardiotoxicity Heatstroke Heatstroke

Ketoacidosis can be divided into mild, moderate and severe according to its degree. Mildness refers to simple ketosis and no acidosis; mild to moderate acidosis can be classified as moderate; Severe refers to ketoacidosis accompanied by coma, or although there is no coma, but the carbon dioxide binding force is less than 10mmol / L, the latter is easy to enter a coma, clinically, the heavier DKA can have the following clinical manifestations:

Symptoms and signs:

1. Diabetes symptoms aggravate and gastrointestinal symptoms

During the DKA compensation period, the patient showed symptoms of the original diabetes such as polyuria, thirst and other symptoms aggravated, obviously fatigue, weight loss; with the progress of DKA, gradually decreased appetite, nausea, vomiting, and even unable to eat water, a small number of patients In particular, children with type 1 diabetes may have extensive acute abdominal pain, with abdominal muscle tension and weakened bowel sounds, and are easily misdiagnosed as acute abdomen. The cause is unknown. It is thought that it may be associated with dehydration, hypokalemia caused by gastrointestinal dilatation or Paralytic ileus and other related, should pay attention to or caused by the rare acute primary intra-abdominal disease that induces DKA, if not the latter, correct the metabolic disorder and relieve abdominal pain.

2. Acidosis, large breath and ketone odor

Also known as Kussmaul breathing, manifested as increased respiratory rate, deep breathing, caused by acidosis, may occur when the blood pH < 7.2, in order to facilitate acid discharge; when the blood pH <7.0, the respiratory center may be inhibited Respiratory paralysis, severe DKA, some patients may have a similar odor of apple odor in their breath.

3. Dehydration and/or shock

In patients with severe DKA, dehydration symptoms and signs are often present. Hyperglycemia leads to a large amount of osmotic diuresis. When acidosis occurs, a large amount of Na in the extracellular fluid is discharged, which makes the dehydration increase in water. When the dehydration amount reaches 5% of body weight, Patients may have signs of dehydration, such as dry skin, lack of elasticity, eyeball and cheek depression, low intraocular pressure, dry tongue and red. If the amount of dehydration exceeds 15% of body weight, there may be circulatory failure. Symptoms include increased heart rate and weak pulse. , blood pressure and body temperature decline, etc., severe cases can be life-threatening.

4. Disorder of consciousness

The clinical manifestations of disturbance of consciousness vary greatly. The early manifestations are lack of energy, dizziness and headache, and then irritability or lethargy, gradually entering drowsiness. All kinds of reflexes disappear from retardation and eventually disappear into coma. The cause of disturbance of consciousness has not yet been elucidated. Dehydration, increased plasma osmotic pressure, dehydration of brain cells and hypoxia have adverse effects on brain tissue function; it is believed that the concentration of ketone bodies in the blood, especially acetoacetate, is too high, which may be closely related to the occurrence of coma, while -hydroxybutyrate Excessive acid accumulation is an important factor leading to acidosis, and acetone is mostly excreted from the breath and its toxicity is small.

5. Induced disease performance

All kinds of induced diseases have their own special performance, should be noted and identified, to avoid confusion with DKA or cover each other and delay diagnosis and treatment.

The diagnosis of DKA is not difficult. The key is to think about the possibility of DKA. DKA is mainly prone to type 1 diabetes. For some children with type 1 diabetes, sometimes it can be misdiagnosed as acute infection or acute abdomen. Pay attention to it, type 2 diabetes is insidious onset, may not be diagnosed after many years of illness, and there are relatively few DKA patients, but in the presence of the above various incentives, even if the patient has no history of diabetes before the disease, DKA occurs.

Examination of diabetic ketoacidosis

Urine sugar, urine ketone positive; blood sugar increased (at 16.7 ~ 33.3mmol / L); white blood cells increased (infection or dehydration); BUN increased, carbon dioxide binding capacity, PH decreased, electrolyte imbalance.

Urine check

(1) Urine sugar: often strong positive, but urine sugar decreased or even disappeared when severe renal function decreased.

(2) Urine ketone body: When the kidney function is normal, the ketone body is often strongly positive, but when the renal function is obviously impaired, the urinary ketone body is reduced or even disappeared. The reagent for qualitative determination of ketone body is reacted only with acetoacetic acid and reacted with acetone. Weak, no reaction with -hydroxybutyric acid, so when the urine is mainly -hydroxybutyric acid, it is easy to miss diagnosis.

(3) Sometimes there may be proteinuria and tubular urine, and the excretion of sodium, potassium, calcium, magnesium, phosphorus, chlorine, ammonium and HCO-3 in the urine increases.

2. Blood test

(1) Blood sugar: The blood sugar is increased, most of which is 16.65 to 27.76 mmol/L (300-500 mg/dl), sometimes up to 36.1-55.5 mmol/L (600-1000 mg/dl) or above, and blood glucose>36.1 mmol/L. Hyperosmolar coma can often be accompanied.

(2) blood ketone: qualitative and strong positive, but because the ketone body in the blood is often -hydroxybutyric acid, the blood concentration is 3 to 30 times that of acetoacetic acid, and parallel to the ratio of NADH/NAD, such as When the blood is mainly -hydroxybutyric acid and the qualitative test is negative, the specific enzyme test should be further carried out to directly measure the -hydroxybutyric acid level. When DKA is used, the blood ketone body is generally quantified above 5 mmoL/L (50 mg/dl). Sometimes it can reach 30mmol/L, more than 5mmol.

(3) Acidosis: mainly related to the formation of ketone bodies including -hydroxybutyric acid, acetoacetic acid and acetone, acetoacetic acid and acetone can react with sodium nitroprusside, and -hydroxybutyric acid and sodium nitroprusside Can not respond, in most cases, DKA, a large amount of acetoacetate in the serum reacted with sodium nitroprusside, the metabolic acidosis of this disease, the compensated pH can be in the normal range, when decompensated, pH Often lower than 7.35, sometimes less than 7.0, CO2 binding force is often lower than 13.38mmol / L (30% volume), severely lower than 8.98mmol / L (20% volume), HCO3- can be reduced to 10 ~ 15mmol / L, blood gas analysis alkali increased, buffer base was significantly reduced (<45mmol / L =, SB and BB also decreased.

(4) Anion gap: reflecting the metabolic acid-base balance, the calculation method is: (Na K )-(Cl- HCO3-), the normal range is 8-12 mmol/L, mainly by the negatively charged albumin and physiological Concentration of organic acids (lactic acid, phosphoric acid, sulfuric acid, etc.). In DKA, due to the increase of ketone body, neutralizing HCO3-, the anion gap increases. If the anion gap increases, it indicates that the organic acid increases. If the patient is diabetic, it indicates DKA. In DKA, serum ketone body qualitative test is often strongly positive. Otherwise, it may suggest that -hydroxybutyric acid is not properly accumulated in the body. The body preferentially produces -hydroxybutyrate in hypoxia and hypoperfusion, such as DKA patients in low In blood pressure or hypoxia, -hydroxybutyric acid is the main body in the body, and the blood ketone body qualitative test can be weakly positive, but with the correction of DKA and the improvement of the condition, the conversion of -hydroxybutyric acid to acetoacetate increases the blood ketone. The body can be strongly positive, but the anion gap is reduced.

(5) Electrolyte:

1 blood sodium: the majority (67%) is lower than 135mmol / L, a small number of normal, even can be raised to 145mmol / L or more, greater than 150mmoLl / L should be suspected with hyperosmolar coma.

2 blood potassium: DKA, because the osmotic diuretic and ketone body is discharged in the form of salt through the kidney, resulting in a large amount of K excreted by the kidney, plus less food, nausea and vomiting, further aggravating the body's potassium deficiency, but DKA, cells The concentration of external hydrogen ions increases with intracellular potassium ion exchange, and intracellular potassium transfers to the outside of the cell; as water migrates from the cell to the outside of the cell, potassium enters the cell at the same time; the loss of phosphorus in the cell leads to the loss of potassium to maintain electrical neutrality. In DKA, insulin deficiency, potassium transfer to the cells decreased, and intracellular glycogen and protein cleavage increased, further promoting the movement of potassium to the outside of the cell. The above various reasons may cause the serum potassium concentration to be normal, even high, thus concealing The real situation of a serious lack of K in the body.

In addition, DKA is often accompanied by phosphorus deficiency and magnesium deficiency.

(6) Blood osmotic pressure: It can be slightly elevated, sometimes up to 330mOsm/L, and a few can reach 350mOsm/L, possibly accompanied by hypertonic dehydration or hyperosmolar coma.

(7) Blood lipids: In the early stage of the disease, free fatty acids (FFA) often increase significantly, about 4 times the normal high limit, up to 2500moL / L; triglycerides (TG) and cholesterol are also significantly increased, TG can reach 11.29mmoL / L (1000mg / dl) or more, sometimes serum is milky white, due to high chylomicronemia, high-density lipoprotein (HDL) often falls to the normal low limit, after insulin treatment, the above lipid metabolism can be abnormal restore.

(8) Serum creatinine and urea nitrogen: often due to loss of water, circulatory failure (prerenal) and renal insufficiency, can be restored after fluid replacement.

(9) Blood routine: The number of white blood cells is often increased, and it can reach (15~30)×109/L without infection, and the neutrophil increase is obvious. The mechanism is unknown, and may be related to the marginal granulosa cells during stress. Released to the circulating pool and concentrated by blood, but often there is no nuclear left shift and poisoning particles. In DKA, clinically, it is not possible to reflect the presence of infection only by white blood cell count and body temperature. Careful search for possible infections, hemoglobin, should be sought. Erythrocyte and hematocrit are often elevated and related to the degree of water loss.

(10) Others: Occasionally, the blood lactate concentration is increased (>1.4mmol/L), shock is more likely to occur in hypoxia, and blood amylase may be slightly elevated, and the marked increase may indicate acute pancreatitis.

According to the condition, you can choose B-ultrasound and electrocardiogram.

Diagnostic diagnosis of diabetic ketoacidosis

Key points for diagnosing DKA

(1) Types of diabetes, such as sudden onset of type 1 diabetes; type 2 diabetes with acute infection or severe stress.

(2) Symptoms and clinical manifestations of ketoacidosis.

(3) The blood glucose is moderately elevated, and the blood osmotic pressure is normal or not very high.

(4) Urine ketone body positive or strong positive, or elevated blood ketone, is one of the important diagnostic basis of DKA.

(5) Acidosis, heavier DKA patients are often accompanied by compensatory or decompensated acidosis, and other causes of acidosis.

2. Critical indicators of diabetic ketoacidosis

(1) Clinical manifestations include severe dehydration, acidosis, breathing and coma.

(2) Blood pH <7.1, CO2CP <10mmol/L.

(3) Blood glucose>33.3mmol/L accompanied by hyperosmosis of plasma.

(4) Electrolyte disorders such as hyperkalemia or hypokalemia.

(5) Blood urea nitrogen continues to increase.

3. Precautions

In order to quickly determine the diagnosis, determine the severity, and find the cause, focus on the medical history and physical examination, pay special attention to the patient's state of consciousness; respiratory frequency and intensity, exhaled odor; degree of dehydration; heart, renal function status; presence or absence of infection and Excited state, etc., and immediately or simultaneously do the necessary laboratory tests.

Differential diagnosis

1. Hyperosmolar non-ketotic diabetic coma: such patients may also have dehydration, shock, coma and other manifestations, more common in the elderly, but blood glucose often exceeds 33.3mmol / L, blood sodium exceeds 155mmol / L, plasma osmotic pressure exceeds 330 mmol / L, blood ketone body was negative or weakly positive.

2. Lactic acidosis: These patients have acute onset, infection, shock, history of hypoxia, acidosis, rapid breathing and dehydration. Although blood glucose is normal or elevated, blood lactate is significantly elevated. (more than 5 mmol/L), the anion gap exceeded 18 mmol/L.

3. Alcoholic acidosis: There are alcohol abuse habits, which are often caused by heavy drinking. The patient's blood -hydroxybutyrate is elevated due to hyperemesis, and blood ketone may be positive, but there is an increase in acidosis and anion gap. Its osmotic pressure also increases.

4. Hunger ketosis: due to insufficient eating, the patient's fat is decomposed, blood ketone is positive, but urine sugar is negative, and blood sugar is not high.

5. Hypoglycemia coma: The patient had had too little food, the onset was acute, and he was sick, coma, but urine sugar, urine ketone negative, low blood sugar, excessive overdose of insulin or excessive intake of hypoglycemic drugs.

6. Acute pancreatitis: More than half of patients with diabetic ketoacidosis will develop blood, and the urinary amylase will increase non-specifically, sometimes with a large increase.

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