Basic Introduction
Characteristics: severe dehydration acidosis electrolyte balance disorders carry oxygen around the circulatory failure system disorders and renal dysfunction nervous dysfunction in patients with rotten apple in the majority of clinical manifestations of disturbance of consciousness occurred a few days before more urine, polydipsia polydipsia and fatigue, subsequent loss of appetite, nausea, vomiting, often accompanied by headache, lethargy, irritability, rapid deep breathing, breath in a rotten apple. With the further development of the disease, severe dehydration, decreased urine output, lethargy and even coma. Diagnosis of DKA diagnosis requires a high blood sugar disease, high blood ketosis and metabolic acidosis performance. If the patient blood or urine glucose, ketones are strongly positive, can be diagnosed with DKA. Began regular blood glucose levels between 400 ~ 800mg / dl (22.2 ~ 44.4mmol / L), but may be higher. plasma pH and bicarbonate decreased, increased anion gap. Initially, the serum sodium decreased slightly, and increased or normal serum potassium often limited. potassium 4.5 mmol / L potassium loss should be considered as a basis for clear, fast potassium needs. At first, blood urea nitrogen (BUN) usually prerenal azotemia increased to the expected value. serum amylase is usually higher, but rare in DKA with pancreatitis . should carefully look for treatable infections. complicati. DKA brain edema has been reported during treat

ment can be symptomatic or even fatal brain edema, common in young adults with symptoms of cerebral edema rare. However, clinical studies reported in DKA treatment within the first 24h, EEG and CT often showed subclinical cerebral edema. More than the blood glucose, serum sodium dropped too quickly, causing rapid decline in blood osmotic pressure and water into the brain cells and brain caused by interstitial; In addition, rapid correction of acidosis, the oxygen away from the curve to the left, central nervous system hypoxia, increased brain edema, abnormal cerebrospinal fluid acidosis and brain edema is also related. The clinical presentation often after treatment, the patient was transferred clear consciousness after the coma again, and often accompanied by injection of vomiting, need to be vigilant, once the diagnosis should be actively rescue treatment to reduce intracranial pressure. 2. Hypokalemia current low-dose insulin therapy, the slower infusion rate and carefully fill the liquid alkali and other improvements in treatment, reducing the extracellular potassium the rate of transfer to the cells, reducing iatrogenic hypokalemia occurred. It should be noted with saline, insulin and glucose infusion and acidosis correction, the four can reduce the serum potassium, as long as the
patient during the treatment of DKA and the case of urine, potassium and should complement the ongoing monitoring potassium. Usually every infusiL, measuring potassium 1, if the amount of ins 0.1U / (kg · h), serum potassium monitoring should be shorter interval. 3. DKA treatment of low blood sugar, blood sugar returned to normal faster than ketoacidosis usually corrected at this time, who continued to insulin, without at the same infusion of glucose, the hypoglycemia. 1h after the start of treatment should be measured for each blood glucose 1, continuous measurement of 4; and then measured every 2h 1 of measured 4 times; then measured every 4h 1. General requirements for blood glucose per hour 3.33 ~ 5.56mmol / L the rate of decline. Once the blood glucose reached 13.9 ~ 16.7mmol / L, the insulin input speed by half, and began to add 5% or 10% glucose liquid, in order to avoid hypoglycemia. 4. DKA treatment of hyperlipidemia in high chlorine recovery process often appear high chlorine hyperlipidemia or high acidosis: DKA when, Cl-loss than the loss of sodium, add saline containing the same amount of Na and Cl-, Chlorine can cause relatively high viremia; DKA recovery, Na and HCO3-transfer to the cells, and Cl-over to remain in the extracellular; DKA recovery, ketone bodies are metabolized anion NaHCO3, lead to high chloride acidosis. DKA treatment, if the normal anion gap gradually, followed by the high chlorine anion gap acidosis in non-general had no clinical significance. 5. Adult respiratory distress syndrome (ARDS) is rare, but may be potential during DKA treatment, fatal complications. When the majority of patients in DKA arterial partial pressure of oxygen (PaO2) and alveolar - arterial oxygen gradient (A-aO2) normal. At this point, because the body's dehydration and NaCl was the lack of colloid osmotic pressure increased in the body, with the added hydration and electrolyte therapy, colloid osmotic pressure were decreased, resulting in significantly lower than normal. With the reduction of colloid osmotic pressure, PaO2 decreased and A-aO2 gradient increased. This is no clinical significance in most patients, will not lead to clinical symptoms and signs, chest X ray normal, and only a small part of the process in the treatment of patients progressed to ARDS. Quickly enter the crystal, increased left atrial pressure and lower plasma colloid osmotic pressure, these changes can be induced pulmonary edema formation, and even heart function under normal circumstances. DKA treatment, the appearance of pulmonary rales and the A-aO2 gradient broadening the risk of ARDS prompted for these patients fluid infusion rate should be reduced, especially in elderly or patients with history of heart disease. Regular monitoring of blood gas analysis and A-aO2 gradient, to help prevent the occurrence of ARDS. 6. Infection is a common complication of DKA. Often due to decreased immunity the body fight infection easily understood concurrent infection. Also easy because of anti-infective use of broad spectrum antibiotics, resulting in some conditions lead to fungal growth of pathogenic bacteria, and fungal infections. 8. Cardiovascular system: too much fluid too fast, can lead to heart failure; loss of potassium or potassium, is easy to arrhythmia, or cardiac arrest; lower blood sugar or low blood sugar too quickly, the heart may occur infarction, and even shock or sudden death; blood concentration, coagulation factors strengthened, can cause cerebral thrombosis, pulmonary embolism and other complications. 9. Acute renal failure: mostly the result of severe dehydration, shock, a serious decline in easily understood concurrent renal circulation of the disease. 11. Serious infections and sepsis: often makes the disease worse, difficult to control, affect the prognosis. 12. Disseminated intravascular coagulation (DIC): severe infection such as sepsis and shock, acidosis, etc., so that concurrency of the disease. 13. Diabetic hyperosmolar coma and lactic acidosis: acid in diabetic ketoacidosis, poisoning may be associated with these two disorders. 14. Other: such as acute pancreatitis, acute gastric dilation. 1 treatment treatment principles: fluid to restore blood volume as soon as possible, correcting dehydration status, lower blood sugar, to correct electrolyte and acid-base balance, and actively look for and eliminate incentives to prevent complications and reduce mortality. The main purpose of the treatment are: (1) rapid expansion; (2) to correct hyperglycemia and high blood ketosis; (3) during treatment to prevent hypokalemia; (4) identification and treatment of bacterial infections. With bicarbonate rapid correction of sodium pH for most patients (plasma 7) is unnecessary, such treatment can induce alkalosis and hypokalemia in serious danger. In the course of DKA treatment of a doctor close observation is necessary, because the frequent Clinical and laboratory evaluation and calibration of appropriate treatment is essential. fatality rate is about 10%, admission hypotension, and coma are unfavorable prognostic factors. Death is mainly due to circulatory failure, hypokalemia and infection. acute cerebral edema, this rare and often fatal complication seen in children, adolescents and young adults less seen. DKA is no evidence of any significant changes in the treatment of acute cerebral edema can be dangerous. Some doctors believe that the rapid blood sugar should be avoided reduction (per 50mg/dl, per 2.78mmol / L), to slow the rapid changes in osmotic pressure. Some patients have aura symptoms (such as sudden headache, rapid change in consciousness), but some patients appear at the outset respiratory arrest. the breathing stopped, the application of high ventilation, steroids, mannitol often ineffective. have been reported cases of individual improvement, and often have lasting neurological dysfunction. rapid infusion of intravenous fluid therapy in adults of 0.9% sodium chloride solution (such as 1L/30min), and then, if blood pressure (BP) stable, adequate urine output, reduced hourly 1L. usually fluid loss 3 ~ 5L, water loss of more than electrolyte loss. When blood pressure is stable, to restore a sufficient amount of urine, the commonly used 0.45 % sodium chloride plus potassium, free water and began to supplement potassium. the general lack of potassium 3 ~ 5mmol / L, serum potassium levels in most patients started or increased upper limit of normal, began to potassium (20 ~ 40mmol / h) usually delayed 2 hours, the hourly measured serum potassium as a guide. because insulin allows the transfer of potassium into cells, when the patient serum potassium 4.5mEq / L, although a metabolic acidosis, once a sufficient amount of urine, potassium as soon as possible and closely monitoring potassium insulin therapy began regular insulin 10 ~ 20u intravenous injection, followed by regular insulin in 0.9% sodium chloride solution to 10u / h infusion rate, the therapeutic dose for most adults is adequate But some people need higher doses. For most children, the first intravenous injection of regular insulin (0.1u/kg body weight) and then regular insulin in 0.9% sodium chloride solution infusion rate per hour 0.1u/kg weight. should be adjusted according to response to treatment of insulin infusion. hour monitoring of blood glucose, insulin effect can be evaluated, and appropriate dose adjustments to make the blood sugar decreased. If the amount of insulin sufficient to lower blood sugar, within a few hours to correct the ketonemia. Blood pH and bicarbonate usually 6 to 8 hours significantly improved, but returned to normal bicarbonate may take up to 24 hours. When the blood sugar dropped to 250 ~ 300mg/dl (13.88 ~ 16.65mmol / L) should use 5 % glucose infusion to reduce the risk of hypoglycemia. At this point you can reduce the insulin dose, but the need to continue regular insulin drip until the blood ketones, urine ketone sustained negative. and then switch to regular insulin subcutaneously, every 4 to 6 Hour 1. DKA recovery in the first 24 hours after the rapid emergence of high insulin may disable ketonemia. When the patient can tolerate should be oral rehydration. prevention of common sense kind of DKA can be prevented acute complications of diabetes, The key to prevention of diabetes in patients with DKA has a high degree of awareness and under the guidance of specialists, a reasonable application of the three major diabetes treatment - diet, exercise, medication, to avoid the occurrence of a variety of incentives such as: infection, stress, etc. adhere to self-care, regular blood glucose, urine sugar and urine ketone body, when blood glu 14mmol / L (250mg/dL), associated with weak-positive urine ketone, the need to immediately, under the guidance of specialists to give sufficient quantities of insulin therapy, not to stage of development to DKA. First aid measures 1) potassium should be positive. 2, due to acidosis within the escape of potassium from the cells, normal serum potassium does not mean that the normal metabolism of potassium, and in fact still lost potassium. Another application of insulin therapy tend to restore blood volume, a large number of rows of potassium in urine, while glucose utilization due to the increase of potassium ions into the cell, because of ketoacidosis was corrected after the cells release hydrogen ions and potassium intake, so this disease in Department lost one of the characteristics of potassium, it should be actively potassium, when the serum potassium is lower than 3.5mmol / L is much loss of potassium, potassium should be positive, such as potassium higher than 5.5mmol / L and accompanied by oliguria or anuria, there are signs of renal insufficiency or suspicious persons, the close observation and Siji considered provisional potassium. About when to start potassium, potassium and glucose in the past most of the water at the same time that the static point, in recent years has become more various opinions ahead of potassium, unless hyperkalemia or renal insufficiency or when no urine, or potassium and insulin at the same time, that is the beginning of rehydration, the same potassium. The amount of potassium 24-hour total of general 6 ~ 10g, preferably potassium or ECG monitoring, slow potassium into the cell, potassium at least 5 to 7 Days to correct the loss of potassium, the current emphasis after the patient can eat potassium to be serving a week. (2) correct acid premature. Acidosis due to the disease is based on the lack
of insulin, ketoacids generated too much, not too much HCO3 loss, it is inhibited by insulin generates ketone bodies to promote the keto acid oxidation, the self-correcting acidosis, it is not too much too early to make up base . Premature and excessive supply of sodium bicarbonate (NaHCO 3) has the following disadvantages: 1) a large number of NaHCO3 often leads to hypokalemia; 2) abnormal cerebrospinal fluid pH decreased; 3) excessive sodium load; 4) response to alkalosis; 5 ) inhibited the dissociation of hemoglobin with oxygen systems caused by tissue hypoxia; 6) lead to cerebral edema. When the pH is greater than 7.1 when it should not make up base, if the pH is lower than 7.1 or carbon dioxide combining power less than 9.0mmol / L when the need to make alkali, sodium bicarbonate, without sodium lactate. Usually give a 5% sodium bicarbonate 100mL, intravenous drip. If the blood is greater than pH7.2 or carbon dioxide combining power 13.5mmol / L to stop the meeting when the base.
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