Transcript of Ketoasidosis Diabetikum. Pengantar Tahun , pasien rawat inap KAD rata-rata lama menginap hari. Kelalaian. Download Citation on ResearchGate | Gambaran Klinis Ketoasidosis Diabetikum Anak | Penelitian ini dilakukan untuk menggambarkan profil klinis ketoasidosis. Penelitian ini dilakukan untuk menggambarkan profil klinis ketoasidosis diabetikum pada anak. Data dikumpulkan dari rekam medik gambaran klinis pasien.
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Diabetic ketoacidosis DKA is a potentially life-threatening complication of diabetes mellitus. DKA happens most often in those with type 1 diabetesbut can also occur in those with other types of diabetes under certain circumstances. The primary treatment of DKA is with intravenous fluids and insulin. Rates of DKA vary around the world.
The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe.
In severe DKA, breathing becomes rapid and of a deep, gasping character, called ” Kussmaul breathing “. On physical examination there is usually clinical evidence of dehydrationsuch as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, a rapid heart rate and low blood pressure may be observed.
MAKALAH Keto Asidosis Diabetikum
Often, a “ketotic” odor is present, which is often described as “fruity”. If Kussmaul respiration is present, this is reflected in an increased respiratory rate. Small children with DKA are relatively prone to brain swellingalso called cerebral edema, which may cause headache, coma, loss of the pupillary light reflexand can progress to death. It occurs in about 1 out of children with DKA and more rarely occurs in adults. DKA most frequently occurs in those who know they ketoawidosis diabetes, but it may also be the first presentation in someone who had not previously been known to be diabetic.
There is often a particular underlying problem kehoasidosis has led to the DKA episode; this may be intercurrent illness pneumoniainfluenzagastroenteritisa urinary tract infectionpregnancyinadequate insulin administration e. Young people with recurrent episodes of DKA may have an underlying eating disorderor may be using insufficient insulin for fear that it will cause weight gain.
Diabetic ketoacidosis may occur in those previously known to have diabetes mellitus type 2 or in those who on further investigations turn out to have features of type 2 diabetes e. Their condition is then labeled “ketosis-prone type 2 diabetes”. Drugs in the gliflozin class SGLT2 inhibitorswhich are generally used for type 2 diabetes, ketoasidowis been associated with cases of diabetic ketoacidosis where the blood sugars are not significantly elevated “euglycemic DKA”.
This may be because they were being used in people with type 1 diabetes, but in those with type 2 diabetes it may be as a result of an increase in glucagon levels. Diabetic ketoacidosis arises because of a lack of diabeetikum in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver a process that is normally suppressed by insulin from glycogen via glycogenolysis and also through gluconeogenesis.
High glucose levels spill over into the urine, taking water and solutes such as sodium and potassium along with it in a process known as osmotic diuresis. The ketone bodies, however, have a low pKa and therefore turn the blood acidic metabolic acidosis.
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The body initially buffers the change with the bicarbonate buffering systembut this system is quickly overwhelmed and other mechanisms must work to compensate for the acidosis. This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.
In various situations such as infection, insulin demands rise but are not matched by the failing pancreas. Blood sugars rise, dehydration ensues, and resistance to the normal effects of insulin increases further by way of a vicious circle.
Glucose fiabetikum usually exceed DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production is present but is insufficient to meet the body’s requirements as a result of end-organ insulin resistance. Usually, these amounts of insulin are sufficient to suppress ketogenesis. If DKA occurs in someone with type 2 diabetes, their condition is called “ketosis-prone type 2 diabetes”.
The clinical state of DKA is associated, in addition to the above, with the release of various counterregulatory hormones such as glucagon and adrenaline as well as cytokinesthe latter of which leads to increased markers of inflammationeven in the absence of infection. Cerebral edema, which is the most dangerous DKA complication, is probably the result of a number of factors. Some authorities suggest that it is the result from overvigorous fluid replacement, but the complication may develop before treatment has been commenced.
Diabetic ketoacidosis may be diagnosed when the combination of hyperglycemia high blood sugarsketones in the blood or on keetoasidosis and acidosis are demonstrated. In addition to the above, blood samples are usually taken to measure urea and creatinine measures of kidney functionwhich may be impaired in DKA as ketoasidozis result of dehydration and electrolytes. Furthermore, markers of infection complete blood countC-reactive protein and acute pancreatitis amylase and lipase may be measured.
Given the need to exclude infection, chest radiography and urinalysis are usually performed. If cerebral edema is suspected because of confusion, recurrent vomiting or other symptoms, computed tomography may be performed to assess its ketoasidosls and to exclude other causes such as stroke. Diabetic ketoacidosis is distinguished from other diabetic emergencies by the presence of large amounts of ketones in blood and urine, and marked metabolic acidosis.
Ketoacidosis is not always the result of diabetes. It may also result from alcohol excess and from starvation ; in both states the diavetikum level is normal or low. Metabolic acidosis may occur in people with diabetes for other reasons, such as poisoning with ethylene glycol or paraldehyde. Attacks of DKA can be prevented in those known to have diabetes to an extent by adherence to “sick day rules”; these are clear-cut instructions to person on how to treat themselves when unwell.
Instructions include advice doabetikum how much extra insulin dixbetikum take when sugar levels appear uncontrolled, an easily digestible diet ketoasidoss in salt and carbohydrates, means to ketoasiosis fever and treat infection, and recommendations when to call for medical help.
People with diabetes can monitor their own ketone levels when unwell and seek help if they ketoazidosis elevated.
The main aims in the treatment of diabetic ketoacidosis are replacing the lost fluids and electrolytes while suppressing the high blood sugars and ketone production with insulin.
Admission to an intensive care unit or similar high-dependency area or ward for close observation may be necessary. The amount of fluid replaced depends on the estimated degree of dehydration.
A special but unusual consideration is diabeti,um shockwhere the blood pressure is decreased not due to dehydration but due to inability of the ietoasidosis to pump blood through the blood vessels.
This situation requires ICU admission, monitoring of the central venous pressure which requires the insertion of a central venous catheter in a large upper body veinand the administration of medication that increases the heart pumping action and blood pressure.
Some guidelines recommend diabeyikum bolus initial large dose of insulin of 0.
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This can be administered immediately after the potassium level is known to be higher than 3. In general, insulin is given at 0. Guidelines differ as to which dose to use when blood sugar levels start falling; some recommend reducing the dose of insulin once glucose falls below Potassium levels can fluctuate severely during the treatment of DKA, because insulin decreases potassium levels in the blood by redistributing it into cells via increased sodium-potassium pump activity.
Ketoasiodsis large part of the shifted extracellular potassium would have been lost in urine because of osmotic diuresis. Hypokalemia low blood potassium concentration often follows treatment. This increases the risk of dangerous irregularities in the heart rate. Therefore, continuous observation of the heart rate is recommended,  as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids once levels fall below 5.
If potassium levels fall below 3. The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is ketoasidosiis. There is little evidence that it improves outcomes beyond diabegikum therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body’s cells and increase the risk of certain complications. Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilationand close observation.
The administration of fluids is slowed. Once this has been achieved, insulin may be switched to the usual subcutaneously administered regimen, one hour after which the intravenous administration can be discontinued.
In people with suspected ketosis-prone type 2 diabetes, determination of antibodies against glutamic acid decarboxylase and islet cells may aid in the decision whether to continue insulin administration long-term if antibodies are detectedor whether to withdraw insulin and attempt treatment with oral medication as in type 2 diabetes. Diabetic ketoacidosis occurs in 4. There has been a documented increasing trend to hospital admissions. The first full description of diabetic ketoacidosis is attributed to Julius Dreschfelda German pathologist working in ManchesterUnited Kingdom.
Numerous research studies since the s have focused on the ideal treatment for diabetic ketoacidosis. The entity of ketosis-prone type 2 diabetes was first fully described in after several ketoasdiosis case reports. It was initially thought to be a form of maturity onset diabetes of the young and went through several other descriptive names such as “idiopathic type 1 diabetes”, “Flatbush diabetes”, “atypical diabetes” and “type 1.
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