The diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes, which is characterized by the appearance of hyperglycemia, hyperketonemia and metabolic acidosis. DKA occurs in the course of type 1 diabetes. It causes nausea, vomiting and abdominal pain and can progress to a life-threatening illness when a cerebral edema, with coma. A DKA is likely at a hyperglycemia with simultaneous hyperketonemia and metabolic acidosis with anion. The treatment consists of volume expansion, insulin substitution and prevention of hypokalemia.
DKA is most common and develops when insulin levels are no longer sufficient in patients with type 1 diabetes to get the basal metabolic needs of the body upright. A DKA is the initial manifestation of the disease in a minority of Type 1 diabetics. Insulin deficiency can be absolute (as in suspending supply exogenous insulin) relative or when normal doses of insulin no longer sufficient to meet the metabolic needs during acute infection, trauma or other physiological stress.
The diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes, which is characterized by the appearance of hyperglycemia, hyperketonemia and metabolic acidosis. DKA occurs in the course of type 1 diabetes. It causes nausea, vomiting and abdominal pain and can progress to a life-threatening illness when a cerebral edema, with coma. A DKA is likely at a hyperglycemia with simultaneous hyperketonemia and metabolic acidosis with anion. The treatment consists of volume expansion, insulin substitution and prevention of hypokalemia. DKA is most common and develops when insulin levels are no longer sufficient in patients with type 1 diabetes to get the basal metabolic needs of the body upright. A DKA is the initial manifestation of the disease in a minority of Type 1 diabetics. Insulin deficiency can be absolute (as in suspending supply exogenous insulin) relative or when normal doses of insulin no longer sufficient to meet the metabolic needs during acute infection, trauma or other physiological stress. Common physiological stress that can trigger DKA are: Acute infections (particularly pneumonia and urinary tract infections) myocardial infarction stroke pancreatitis injuries are medications that can be involved in the development: corticosteroids thiazide diuretics sympathomimetic A DKA is much less common in type 2 diabetics but may well occur in situations of unusual stress. Pathophysiology A lack of insulin causes the body to metabolize glucose for energy in place of the triglycerides, and amino acids. The serum levels of glycerol and free fatty acids (FFA) rise due to the increased lipolysis. The same is true because of muscle catabolism for alanine. Glycerol and alanine are substrates of hepatic gluconeogenesis, which is stimulated by the excessive glucagon secretion, which is associated with insulin deficiency. Glucagon stimulates the mitochondrial conversion of FFA into ketones. Insulin normally prevents ketogenesis by inhibition of the transport of FFA derivatives in the mitochondrial matrix; in the absence of insulin occurs progression ketogenesis. The main produced ketone bodies, acetoacetic acid and ?-hydroxybutyric acid, are strong organic acids that cause metabolic acidosis. Acetone from the metabolism of acetoacetic cumulated in serum and exhaled slowly. Hyperglycemia, which is caused by a lack of insulin, leading to osmotic diuresis, which in turn caused a significant renal loss of water and electrolytes. The excretion of ketones in the urine caused an additional loss of sodium and potassium. The serum sodium may drop by the natriuresis or rise due to the excretion of large amounts of free water. Potassium is also lost in large quantities, sometimes h> 300 mEq / 24 hours. Despite the significant potassium deficiency with respect to the total body amount is increased at the beginning of potassium levels typically as it comes because of the acidosis to a Kaliumeinstrom in the extracellular space. Potassium levels continue to fall over the course of therapy since insulin leads to the uptake of potassium into cells. If not, the serum potassium values ??are checked and if necessary is substituted potassium, is life-threatening Hypokalämien can develop. Symptoms and signs The symptoms of DKA are those of hyperglycemia (diabetes mellitus (DM): symptoms and complaints) with the additional incidence of nausea, vomiting and – especially in children – abdominal pain. Lethargy and drowsiness are symptoms of an already severe decompensation. Patients can hypotonic by the dehydration and acidosis and his tachycardic; breathe quickly and deeply, to compensate for the acidemia (Kussmaul breathing). The exhaled air can smell fruity because of the exhaled acetone. Fever is not an independent symptom of DKA, but, if present, indicate a causal infection. Without timely treatment, the DKA can to progress to coma and death. The acute cerebral edema, a complication that occurs in 1% of DKA patients, mainly affects children and rarely teenagers and young adults. Headaches and changing states of consciousness are harbingers of this complication in some patients, in others it comes as a first manifestation of a respiratory arrest. The cause is still largely unknown, probably the excessively rapid lowering of the serum osmolality or cerebral ischemia plays a role. Cerebral edema occurs with the highest probability in children <5 years if a DKA is the initial manifestation of diabetes mellitus. Children with the highest levels of blood urea nitrogen (BUN) and the lowest PaCO2 on admission appear to have the greatest risk. Delays in the correction of hyponatremia and the use of HCO3 during treatment of DKA are additional risk factors. Diagnosis Arterial pH serum ketones calculation of anion gap in patients with suspected DKA: should be measured serum electrolytes, urea nitrogen and creatinine, glucose, ketones and osmolarity. The urine should be tested for ketones. In patients with shortness of breath blood gases should be measured. DKA is diagnosed when the arterial pH <7.30 with an anion gap> (anion gap) is 12 and if Serumketone be detected at a hyperglycemia. The preliminary diagnosis can be made when glucose and ketones are strongly positive in urine. Urine test strips and some assays for Serumketone may underestimate the extent of ketosis, since they indicate acetoacetic acid and not ?-hydroxybutyric acid, which is normally the predominant acid. Clinical Calculator: anion gap symptoms and signs of causing disease should be investigated by appropriate tests (cultures, imaging, for example.). In adults, an ECG for the detection of acute MI and for the resolution of anomalies in serum K should be done. Other biochemical deviations are hyponatremia, elevated serum creatinine and increased serum osmolality. Hyperglycemia may cause dilutionale hyponatremia, so that the measured serum sodium value is corrected by 100 mg / dL increase in serum glucose above 100 mg / dl is added 1.6 mmol / l. To illustrate this, it is necessary for a patient with a serum sodium value of 124 mEq / and a glucose value of 600 mg / dl exactly 1.6 ([600 – 100] / 100) = 8 mmol / l to 124 add the corrected serum Na of 132 mmol / l. If acidosis is corrected, the potassium level drops. A potassium level <4.5 mEq / L indicates a significant potassium deficiency and requires an immediate substitution. Serum amylase and lipase are often increased, even when no pancreatitis exists. Pancreatitis can be made with additional alcohol disease and hypertriglyceridemia in patients. Prognosis Mortality rates for DKA are between 1 and 10%. Shock or coma at admission provide poorer outcomes. The main causes of death are cardiovascular failure, hypokalemia and infection. Of the children with a cerebral edema 57% recover without residuals, 21% survive with a neurological deficit and 21% die. Intravenous treatment 0.9% saline correction of hypokalemia intravenous insulin (as long as serum potassium is at a value of ? 3.3 mmol / l) Rare i.v. NaHCO3 (if the pH after 1 hour treatment at <7 rests) The measures immediately performed and the initial therapy is faster i.v. Fluid replacement, correction of hyperglycemia and acidosis and timely compensation of hypokalemia. The identification of precipitating factors is also important. Treatment should take place in an intensive care since the beginning hourly and later two-hourly clinical and laboratory assessments with appropriate therapy adjustment is necessary. Intravascular volume should be restored quickly to increase blood pressure and ensure the glomerular perfusion; once the intravascular volume is restored, the remaining liquid shortage affecting the whole body is offset slower h usually over about 24 hours. The initial fluid replacement in adults is carried out with the aid of a rapid infusion of 1-3 l of 0.9% saline. Followed by a continuous infusion of saline at a running rate of 1 l / h or faster, as required, to raise the blood pressure, to correct the hyperglycemia and to maintain adequate urine output upright. Adults with a DKA typically need a minimum of 3 L of brine in the first 5 h. If the blood pressure stable and the urine output is sufficient, the saline is exchanged for a 0.45% saline solution. In fall in plasma glucose concentration to values ??<200 mg / dl (11.1 mmol / l) should be saline, the intravenous fluid from 5% dextrose in 0.45%. Clinical Calculator: Calculate the maintenance requirement of fluid in children for children are estimated deficits liquid at 60 to 100 ml / kg body weight. Maintenance fluids (for current losses) must also be provided (dehydration in children: maintenance requirement). The initial fluid replacement should be done with 0.9% saline (20 ml / kg) over 1-2 h, followed by 0.45% saline solution, when the blood pressure stable and the urine output is sufficient. The remaining liquid deficiency should be replaced about 36 hours, usually at a rate (including the amounts for the maintenance) of 2- 4 ml / kg / h, depending on the degree of dehydration. Hyperglycemia is treated by the i.v. administration of a Normalinsulinbolus in a dosage of 0.1 units / kg. Followed by a continuous infusion of 0.1 unit / kg in 0.9% saline. The insulin should be administered up to a serum potassium are exposed ? 3.3 mEq / l. (Non-ketotic hyperosmolar syndrome (NKHS): Treatment). A Insulinadsorption of infusion tubes can lead to difficult to predict effects. It is recommended that vorzuspülen the infusion tubing at the start of therapy with an insulin solution. In Germany infusions an albumin additive is added. If the plasma glucose values ??fall within the first hour not to 50-75 mg / dl (2.8 to 4.3 mmol / l), the insulin dose should be doubled. With or without bolus children should receive a continuous insulin infusion at a dose of 0.1 U / kg or higher. The ketones should fall within hours if a sufficient dose of insulin is administered. Nevertheless, can create the impression that the drop of the ketones insufficiently proceeds, since it comes to acetoacetic acid with decreasing acidosis to a conversion of ?-hydroxybutyric acid (which is the "ketone", which is measured in most laboratories). Serum pH and HCO3- concentration should quickly improve. However, the restoration of normal serum HCO3- concentration can take 24 hours. Rapid correction of pH by HCO3- gift can be considered when the pH remains an hour after the initial fluid replacement in <7th However HCO3 is associated with the development of an acute cerebral edema and therefore should not be used routinely. If this is used, only a small increase in pH should be attempted (target pH of about 7.1), at dosages of 50-100 mEq over 30-60 min, followed by repeated measurements of arterial pH and serum K. When the plasma glucose levels in adults approach the limit of 200 mg / dl (<11.1 mmol / l), the infusion solution to reduce the risk of hypoglycemia 5% dextrose should be added. The insulin dose can then be reduced to 0.02 to 0.05 units / kg / h. The continuous infusion of insulin, however, should necessarily continue until the anion gap is approaching again and samples are repeatedly tested both blood and urine negative for ketones. Insulin substitution can then s.c. to the administration of 5-10 units of regular insulin every 4-6 hours to be changed. If the patient is stable and able to eat again, either started a conventional insulin therapy (eg. As separate administration of short- or rapid-acting and intermediate or long-acting insulins) or an insulin plan after basal-bolus principle. I.v. infusion of insulin should h for 1-4 after the first s.c. Application of insulin will continue. Children should as long as a continuous insulin infusion at a dose receive 0.05 units / kg / h until the s.c. Administration of insulin is started and the pH is> 7.3. To prevent a hypokalemia and obtaining serum potassium values ??4-5 mEq / l 20-30 mEq of potassium per liter infusion solution must be added. If the serum potassium is <3.3 mEq / L, the insulin infusion was stopped and potassium in a dose of 40 mEq / h are substituted until the serum potassium be ? 3.3 mEq / l. Rising potassium levels> 5 mEq / L, the potassium replacement should be stopped. Normal or elevated levels of potassium at the beginning of therapy reflect the acidosis caused by the shift of intracellular potassium into the extracellular space and disguise the real potassium deficit that almost all DKA patients. Insulin substitution ensures rapid redistribution of potassium into the intracellular space, so potassium levels should be monitored every hour or every two hours at the start of therapy. Hypophosphatemia often develops during treatment of DKA, but the phosphate recovery in most cases of unclear benefit. If indicated (. For example, when rhabdomyolysis, hemolysis or neurological deterioration occurs), K-phosphate and phosphate can be in the ratio of 1: about 6-12 h to be infused. 2 If K-phosphate is given in serum calcium levels decline in general and should be monitored. Treatment of suspected cerebral edema is an early stage of hyperventilation, corticosteroids and mannitol, but these are ineffective often after a respiratory arrest. Summary Acute physiological stressors (eg. As infections, MI) may trigger type 1 diabetes acidosis, moderate increase in glucose levels, dehydration and severe potassium loss in patients. The acute cerebral edema is a rare complication that occurs in 1% of DKA patients. It mainly affects children and rarely teenagers and young adults. DKA is diagnosed when the arterial pH is <7.30 with an anion gap> 12 and if Serumketone be detected at a hyperglycemia. Acidosis can usually with i.v. Liquid and insulin are corrected. A HCO3 administration may be considered when the acidosis (pH <7) after 1 hour of therapy significantly persists. With insulin should be maintained until the serum potassium is 3.3 mmol / l at ?.