I. Overview
Diabetic ketoacidosis (DKA) is a syndrome of hyperglycemia, hyperketosis, ketonuria, dehydration, electrolyte disorders, metabolic acidosis and other pathological changes in diabetic patients due to significant insulin deficiency and inappropriate elevation of gluconeogenic hormones under the effect of various causative factors, which is a common acute complication of diabetes.
This disease is common in patients with type 1 and severe stage 2 diabetes, and the mortality rate accounts for about 10% of the death rate of diabetic patients. Currently, the direct mortality rate of DKA has decreased significantly in most areas of China, and depends largely on timely diagnosis and appropriate treatment. Yang Xiaoxia, Department of Endocrinology, Longyan Second Hospital
Ketoacidosis can be divided into 3 conditions according to its degree: mild, moderate and severe. Mild actually refers to simple ketosis with no acidosis; those with mild or moderate acidosis can be classified as moderate; and severe refers to those with ketoacidosis with coma, or those without coma but with carbon dioxide binding capacity below 10 mmol/L, the latter of which can easily enter coma.
Clinical manifestations
1. There are often obvious causative factors, such as infection, improper diet or treatment and various stress factors. In untreated type 1 diabetic patients with rapid progression, especially in children or adolescents, DKA can be the first symptom to be diagnosed.
2, the symptoms of the original disease sharply aggravated: irritable thirst, polyhydramnios, polyuria (or oliguria),; with the progression of DKA, the gradual appearance of loss of appetite, nausea, vomiting, abdominal pain, and even the inability to eat and drink.
3, there are obvious signs: (1) dehydration signs: dry skin, reduced elasticity, sunken eyes, dry mouth, red lips (like cherry red), tongue like beef, accelerated respiratory rate, deep breathing, exhaled gas with ketone smell (rotten apple smell); (2) peripheral circulation failure: tachycardia, cold extremities, weak pulse, decreased blood pressure, oliguria, anuria or even shock.
4. Disorders of consciousness: clinical manifestations vary greatly among individuals. Early manifestation is mental incompetence, dizziness and headache, followed by restlessness or drowsiness, and gradually enter into coma, and various reflexes are dull and even disappear, and finally enter into coma.
5.Auxiliary examination.
Positive urine glucose and urine ketones.
Increased blood glucose, mostly in the range of 16.7-33.3 mmol/L, and elevated blood ketone bodies.
Blood gas analysis suggestive of metabolic acidosis with decreased carbon dioxide binding capacity.
Blood creatinine and urea nitrogen: mostly elevated, recoverable after rehydration.
III. Diagnostic basis
1, there are often triggers present: more than 80% of DKA episodes have identifiable triggers such as infection, inappropriate drug application, stress, etc.
2.Symptoms and clinical manifestations of ketoacidosis: such as aggravation of the original diabetic symptoms, dehydrated appearance, deep and rapid breathing, and altered consciousness.
3, moderately elevated blood glucose (16.6-33.3mmol/L), normal or not very high blood osmolality.
4, positive or strong positive urinary ketone bodies, or elevated blood ketones, is one of the important diagnostic bases of DKA.
5, acidosis, more severe DKA patients are mostly accompanied by compensated or decompensated acidosis, and exclude other causes of acidosis.
Note: In order to quickly determine the diagnosis, determine the severity and find the causative factors, we should focus on history and physical examination, paying special attention to the patient’s state of consciousness; respiratory rate and intensity, exhaled odor; degree of dehydration; cardiac and renal function status; presence of infection and stress status, etc. And immediately or simultaneously do the necessary laboratory tests.
IV. Treatment principles and methods
Take corresponding treatment measures according to the degree of acidosis: for mild ketoacidosis patients should be encouraged to eat and drink and use sufficient insulin to facilitate the decline of blood sugar and the elimination of ketone bodies; moderate or severe ketoacidosis should be treated with low-dose insulin therapy, and correct the water, electrolyte and acid-base balance when necessary.
1, remove the cause: such as timely application of antibiotics to control infections, etc. The removal of the cause should be throughout the treatment: it is not only conducive to the treatment and remission of DKA, but also can prevent the recurrence of ketoacidosis.
2, general measures.
(1) Draw blood specimens and send them for the laboratory tests required for the diagnosis and treatment of DKA, such as blood glucose, blood ketones, blood pH and CO2CP, BUN, Cr, Na+, K+, Cl- and blood gas analysis. And leave the needle immediately connected to the infusion device.
(2) Collect urine specimen, record urine volume, and send for urine glucose, urine ketones, and urine routine. The catheter is left in place after catheterization in comatose patients to record hourly and 24h urine volumes, and urine can be taken on demand to monitor changes in urine glucose and urinary ketones during treatment.
(3) Comatose patients, or those with vomiting, abdominal distension, gastric retention, or gastric dilatation, should have a gastric tube inserted, continuous gastrointestinal decompression or suction once every 2 hours, record the amount of gastric fluid, and note changes in gastric fluid color and other changes.
(4) According to the first level of care, closely observe the changes of the four vital indicators of T, P, R and BP; accurately record the amount of water in and out and the hourly urine volume; keep the airway open, and give oxygen if the oxygen saturation is <80mmHg.
3.Small dose insulin therapy: The main factor of DKA is insulin deficiency, so the key to treatment is to rapidly supplement insulin to correct the acute metabolic disorder caused by hyperketonemia and acidosis at this time. Since the 1970s, the clinical application of low-dose insulin therapy has been recommended.
Method: The first shock amount of insulin is 12-20U intravenously, and then adults are given 0.1U/kg body weight per hour [0.25U/(kg・h) for children], that is, 4-6U/h, generally not more than 10U/h, so that blood glucose drops at a rate of 4.2-5.6 mmol/h and ketone bodies are eliminated. If the rate of blood glucose drop is less than 30% of the pre-drip level, it indicates that it may be accompanied by anti-insulin factors, and the insulin dosage can be doubled at this time.
When blood glucose drops to 13.9mmol/L, the infusion of 5% glucose (or sugar saline) should be changed to prevent hypoglycemia (because hypoglycemia is not conducive to the elimination of ketone bodies), and insulin (U):glucose (g) = 1:2 to 1:4 (5% glucose 500ml + RI 6-12U) can be administered. At this concentration, the patient’s blood glucose is maintained at about 10 mmol/L by continuous drip, until the urine ketone body turns negative and urine sugar (+) can be transitioned to subcutaneous injection treatment on weekdays.
4. Rehydration: It is especially important for severe DKA, not only for the correction of dehydration, but also for the decrease of blood glucose and the elimination of ketone bodies.
Total amount of rehydration fluid: generally estimated at 10% of the patient’s body weight (kg), the general water loss in adults with DKA 4-6L.
Type of rehydration fluid: start with saline, if blood glucose is not severely elevated 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 facilitate the elimination of ketosis.
The speed of rehydration: according to the principle of first fast 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, up to 2/3 of the total infusion. the rest should be replenished in 24-28h.
5.correct electrolyte disorders: mainly potassium supplementation, or magnesium and phosphorus supplementation as appropriate; the overall potassium loss of patients in DKA is serious, usually reaching 300~1000mmol/L. Due to the use of insulin and the increase of blood pH after acidosis correction, K+ can be promoted to enter the cells; blood volume supplementation can also produce diuretic potassium excretion, thus aggravating potassium deficiency.
Total amount of potassium supplementation: 6-10g for 24h, and the hourly input should not exceed 1.5g (equivalent to 20mmol/L).
Potassium supplementation preparations: intravenous input is commonly used 10% potassium chloride solution, added to liquid 500ml drip, not directly intravenous injection. Oral potassium chloride or 10% potassium citrate can be used to reduce the amount of intravenous potassium supplementation.
Potassium supplementation indications and speed: Unless the patient has renal insufficiency, no urine or high blood potassium (>6.0mmol/L), potassium supplementation should be suspended (at this time, potassium can be supplemented in the second and third infusion as appropriate), generally, intravenous potassium supplementation should be performed after the start of infusion, intravenous insulin and the patient has urine (>30ml/h). In other words, if the blood potassium is low or normal before treatment and the urine volume is >40ml/h, the potassium should be supplemented immediately after the infusion is started; if the patient is conscious, oral potassium chloride or potassium citrate should be given at the same time after the treatment is started.
Continue to take potassium salt 1.0g/time, 3~4 times/d for 7~10 days after DKA is relieved. Monitor the blood potassium level, urine volume and ECG during treatment, and adjust the dosage in time to prevent cardiac arrest caused by high blood potassium.
6. Correction of acidosis: It is not necessary to input alkaline drugs for mild acidosis, and it must be emphasized that only those with severe acidosis need alkaline supplementation. The indications for alkaline supplementation are: severe acidosis, i.e. blood pH <7.1, or HCO3- <10mmol/L, or CO2CP <10mmol/L, should be given alkaline supplementation only.
Type and dose of alkaline supplementation: 5% sodium bicarbonate is commonly used instead of sodium lactate to avoid aggravating the possible lactic acidosis. The dosage is usually 100-200 ml of 5% sodium bicarbonate (2-4 ml/kg body weight), which is diluted into 1.25% isotonic solution for intravenous infusion.
Note that in the input of alkaline solution, avoid using the same pathway with insulin to prevent the decrease of insulin potency, . When blood pH ≥ 7.2 or CO2CP ≥ 15 mmol/L, alkaline supplementation should be stopped.