Diabetic ketoacidosis ( DKA ) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, wheezing, increased urination, weakness, confusion, and sometimes loss of consciousness. One's breath can develop a certain odor. The onset of symptoms is usually rapid. In some cases people may not realize that they previously had diabetes.
DKA is most common in those with type 1 diabetes, but it can also occur in those with other types of diabetes under certain conditions. Triggers may include infection, not taking insulin properly, stroke, and certain medications such as steroids. DKA results from insulin deficiency; as the body's response shifts to the burning of fatty acids that produce acidic ketone bodies. DKA is usually diagnosed when the test finds high blood sugar, low blood pH, and ketoacids either in the blood or urine.
The main treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. During the treatment of blood sugar and potassium levels should be checked regularly. Antibiotics may be needed in those with underlying infections. In those with very low blood pH, sodium bicarbonate may be administered; However, its use is unclear and usually not recommended.
DKA rates vary across the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA every year, while in Malaysia this affects about 25% per year. DKA was first described in 1886 and, until the introduction of insulin therapy in 1920, it was almost universally fatal. The risk of death with adequate and timely treatment is currently about 1-4%.
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Signs and symptoms
Symptoms of diabetic ketoacidosis episodes usually evolve for about 24 hours. The dominant symptoms are nausea and vomiting, thirst being pronounced, excessive urine production and possibly severe abdominal pain. In severe DKA, the breath becomes fast and deep and panting, called "Kussmaul breathing". The abdomen may feel tender to the point that may be suspected by a serious abdominal condition, such as acute pancreatitis, appendicitis or gastrointestinal perforation. A blood vomit resembling a coffee powder occurs in a small number of people and tends to stem from esophageal erosion. In severe DKA, there may be confusion or decrease in alertness marked, including coma.
On physical examination there is usually clinical evidence of dehydration, such as dry mouth and reduced skin turgor. If dehydration is deep enough to cause a decrease in circulating blood volume, rapid heart rate and low blood pressure can be observed. Often, the smell of "ketotis" is present, which is often described as "fruit". If Kussmaul respiration is present, this is reflected in an increase in respiratory rate.
Young children with DKA are relatively susceptible to brain swelling, also called cerebral edema, which can cause headaches, coma, loss of pupil light reflex, and can progress to death. This occurs in about 1 in 100 children with DKA and is less common in adults.
Maps Diabetic ketoacidosis
Cause
DKA most commonly occurs in those who know they have diabetes, but it may also be the first presentation to someone previously unknown to diabetes. There are often certain underlying issues that cause DKA episodes; this may be a coexisting illness (pneumonia, influenza, gastroenteritis, urinary tract infection), pregnancy, inadequate insulin administration (eg damaged insulin transmitters), myocardial infarction (heart attack), stroke or cocaine use. Young people with recurrent DKA episodes may have an underlying eating disorder, or may use insufficient insulin for fear that it will cause weight gain.
Diabetic ketoacidosis can occur in those previously known to have type 2 diabetes mellitus or in those who in further studies have shown a picture of type 2 diabetes (eg obesity, strong family history); this is more common in Africans, African-Americans and Hispanics. Their condition was then labeled "ketosis prone to type 2 diabetes".
Drugs in the class of gliflozine (SGLT2 inhibitor), commonly used for type 2 diabetes, have been associated with cases of diabetic ketoacidosis in which blood sugar did not increase significantly ("euglycemic DKA"). This may be because they are used in people with type 1 diabetes, but in those with type 2 diabetes may be the result of elevated glucagon levels.
Mechanism
Diabetic ketoacidosis arises from lack of insulin in the body. The lack of insulin and an appropriate increase in glucagon lead to increased release of glucose by the liver (a process normally suppressed by insulin) from glycogen through glycogenolysis as well as through gluconeogenesis. High glucose levels spill into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis. This causes polyuria, dehydration, and polydipsia. The absence of insulin also leads to the release of free fatty acids from the adipose tissue (lipolysis), which is altered through a process called beta oxidation, again in the liver, into a ketone body (acetoacetate and? -hydroxybutyrate). ? -Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of famine. The ketone body, however, has a low pKa and hence alters blood acid (metabolic acidosis). The body initially buffered the changes with the bicarbonate buffer system, but the system was quickly overwhelmed and other mechanisms had to work to offset the acidosis. One such mechanism is hyperventilation to lower blood carbon dioxide levels (a form of compensatory respiratory alkalosis). This hyperventilation, in its extreme form, can be observed as Kussmaul respiration.
In various situations such as infection, the need for insulin increases but does not match the pancreas that fails. Blood sugar increases, dehydration occurs, and resistance to the normal effects of insulin rises further through a vicious cycle.
As a result of the above mechanism, the average adult with DKA has a total body water deficiency of about 6 liters (or 100 mL/kg), in addition to substantial deficiencies in sodium, potassium, chloride, phosphate, magnesium and calcium. Glucose levels usually exceed 13.8 mmol/L or 250 mg/dL.
DKA is common in type 1 diabetes because this form of diabetes is associated with an absolute lack of insulin production by the island of Langerhans. In type 2 diabetes, insulin production is present but not sufficient to meet the body's needs as a result of end-organ insulin resistance. Usually, this amount of insulin is enough to suppress ketogenesis. If DKA occurs in someone with type 2 diabetes, the condition is called "ketosis prone to type 2 diabetes". The exact mechanism for this phenomenon is unclear, but there is evidence of both insulin secretion disorders and insulin action. Once the condition has been treated, insulin production is continued and often the person can resume diet or tablet treatment as is usually recommended in 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 and cytokines, the latter leading to an increase in inflammatory markers, even in the absence of infection.
Cerebral edema, which is the most dangerous DKA complication, may be the result of a number of factors. Some experts suggest that this is the result of excessive fluid replacement, but complications may develop before treatment begins. More likely on those with a more severe DKA, and in the first episode of DKA. Possible factors in the development of cerebral edema are dehydration, acidosis and low levels of carbon dioxide; In addition, increased levels of inflammation and coagulation can, along with these factors, lead to decreased blood flow to the part of the brain, which then swells up after fluid replacement has begun. Swelling of brain tissue leads to an increase in intracranial pressure that eventually leads to death.
Diagnosis
Investigation
Diabetic ketoacidosis can be diagnosed when a combination of hyperglycemia (high blood sugar), ketones in the blood or in urinalysis and acidosis are shown. About 10% of cases of blood sugar did not increase significantly ("euglycemic diabetic ketoacidosis").
Arterial blood gas measurements are usually performed to indicate acidosis; This requires taking blood samples from the arteries. Subsequent measurements (to ensure effective treatment), can be taken from normal blood tests taken from the veins, as there is little difference between arterial and venous pH. Ketones can be measured in urine (acetoacetate) and blood (? -hydroxybutyrate). When compared with acetoacetate urine test, determination of capillary content? -hydroxybutyrate may reduce the need for admission, shorten hospital admission duration and potentially reduce hospitalization costs. At very high levels, the measurement of capillary blood ketones becomes imprecise.
In addition to the above, blood samples are usually taken to measure urea and creatinine (a measure of renal function, which may be impaired in DKA due to dehydration) and electrolytes. Furthermore, infection markers (full blood count, C-reactive protein) and acute pancreatitis (amylase and lipase) can be measured. Given the need to exclude infection, chest radiographs and urinalysis are usually performed.
If cerebral edema is suspected due to confusion, recurring vomiting or other symptoms, computed tomography may be performed to assess its severity and to exclude other causes such as stroke.
Criteria
Diabetic Ketoacidosis is distinguished from other diabetes emergencies in the presence of large amounts of ketone in the blood and urine, and marked metabolic acidosis. The hyperglycemic hyperosmolar state (HHS, sometimes labeled "hyperosmolar non-ketotic state" or HONK) is much more common in type 2 diabetes and has an increase in plasma osmolarity (above 320 m/kg) due to dehydration and very deep blood concentrations; mild acidosis and ketonemia may occur in these circumstances, but not to the extent observed in DKA. There is a degree of overlap between DKA and HHS, as in DKA osmolarity can also be increased.
Ketoacidosis is not always the result of diabetes. It may also be the result of excess alcohol and from starvation; in both countries of normal or low glucose levels. Metabolic acidosis may occur in diabetics for other reasons, such as poisoning with ethylene glycol or paraldehyde.
The American Diabetes Association categorizes DKA in adults into one of three stages of severity:
- Light: The blood pH slightly decreases to between 7.25 and 7.30 (normal 7.35-7.45); serum bicarbonate decreases to 15-18 mmol/l (normal above 20); people are wary
- Medium: pH 7,00-7,25, bicarbonate 10-15, mild drowsiness may exist
- Severe: pH below 7.00, bicarbonate below 10, fainting or coma may occur
The 2004 European Community Endocrinology Statement for Child Endocrinology and Lawson Wilkins Pediatric Endocrine Society (for children) use slightly different cutoffs, where mild DKA is defined by pH 7,20-7,30 (bicarbonate 10-15 mmol/l), DKA moderate based on pH 7.1-7.2 (bicarbonate 5-10) and heavy DKA with pH & lt; 7.1 (bicarbonate below 5).
Prevention
DKA attacks can be prevented in those who are known to have diabetes to some extent by adherence to the "rules of sick days"; this is a clear hint to people about how to treat yourself when it's not healthy. Instructions include suggestions about how much extra insulin to take when the sugar levels appear uncontrolled, salt-and-carbohydrate-rich foods, meaning to suppress fever and treat infections, and recommendations when to seek medical help.
Diabetics can monitor their own ketone levels when unhealthy and seek help if they increase.
Management
The main goals in the treatment of diabetic ketoacidosis are replacing lost fluids and electrolytes while suppressing high blood sugar and production of ketones with insulin. Admission to an intensive care unit or area with a high dependence or similar environment for close observation may be required.
Fluid replacement
The amount of fluid replaced depends on the degree of dehydration expected. If dehydration is so severe that it causes shock (blood pressure greatly decreases with inadequate blood supply to the organs), or a decreased level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in recurrent doses for children ) is recommended to restore the circulation volume. Slower rehydration based on calculations of water and sodium deficiency may be possible if dehydration is moderate, and again saline is the recommended fluid. Very mild ketoacidosis without vomiting and mild dehydration can be treated with oral and subcutaneous rehydration rather than intravenous insulin under observation for signs of damage.
Special but unusual considerations are cardiogenic shock, in which blood pressure decreases not because of dehydration but because of the inability of the heart to pump blood through the blood vessels. This requires ICU care, central venous pressure monitoring (requiring insertion of central venous catheters in large upper venous bodies), and administration of drugs that enhance the pumping action of the heart and blood pressure.
Insulin
Some guidelines recommend bolus (large dose of initial) insulin 0.1 unit of insulin per kilogram of body weight. This may be administered as soon as potassium levels are known to be higher than 3.3 mmol/l; if the levels are lower, insulin administration may lead to very low potassium levels (see below). Other guidelines recommend delaying initiation of insulin until fluid has been given. It is possible to use injections of fast-acting insulin analogues under the skin for mild or moderate cases.
In general, insulin is given at 0.1 units/kg per hour to reduce blood sugar and suppress the production of ketones. Different guidelines for which doses are used when blood sugar levels begin to fall; some recommend to reduce the dose of insulin after glucose falls below 16.6 mmol/l (300 mg/dl) but recommend others to include glucose other than salt to allow a higher dose of insulin dose.
Potassium
Potassium levels can fluctuate severely during DKA treatment, because insulin lowers potassium levels in the blood by redistributing into cells through increased activity of the sodium-potassium pump. Most of the extracellular potassium shifts will be lost in the urine due to osmotic diuresis. Hypokalemia (low blood potassium concentration) often follows treatment. This increases the risk of dangerous aberration in the heart rate. Therefore, continuous monitoring of the heart rate is recommended, as well as repeated measurements of potassium and potassium addition to intravenous fluids once the rate falls below 5.3 mmol/l. If potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to allow for correction of hypokalemia.
Bicarbonate
Administration of sodium bicarbonate solution to rapidly increase the level of acid in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that although it can increase blood acidity, it can actually aggravate acidity in the body's cells and increase the risk of certain complications. Therefore, its use is not recommended, although some guidelines recommend it for extreme acidosis (pH & lt; 6.9), and smaller amounts for severe acidosis (pH 6.9-7.0).
Cerebral edema
Cerebral edema, when associated with coma, often requires admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not enforced, but intravenous mannitol and hypertonic saline (3%) are used - as in some other forms of cerebral edema - in an attempt to reduce swelling.
Resolution
DKA resolution is defined as general improvement in symptoms, such as the ability to tolerate nutrients and oral fluids, normalization of blood acidity (pH & gt; 7.3), and the absence of ketones in the blood (& lt; 1 mmol/l) or urine. Once this is achieved, insulin can be transferred to a common subcutaneous regimen, an hour after intravenous administration may be discontinued.
In people with type 2 diabetes who are suspected of ketosis, the determination of antibodies to glutamic acid decarboxylase and islet cells may help in the decision whether to continue long-term insulin administration (if antibodies are detected), or whether to withdraw insulin and try treatment with oral medications such as diabetes type 2. In general, routine measurement of C-peptide as a measure of insulin production is not recommended unless there is doubt, whether a person has type 1 or type 2 diabetes.
Epidemiology
Diabetic ketoacidosis occurs in 4.6-8.0 per 1,000 people with diabetes each year. The rate among those with type 1 diabetes is higher with about 4% in the UK developing DKA a year while in Malaysia conditions affect about 25% per year. In the United States, 135,000 hospital admissions occur annually as a result of DKA, with an estimated cost of $ 2.4 billion or a quarter to a half of the total cost of care for people with type 1 diabetes. There has been a documented improvement trend for hospital admissions. Risks are increased in those with sustained risk factors, such as eating disorders, and those unable to afford insulin. About 30% of children with type 1 diabetes receive their diagnosis after one episode of DKA.
Previously considered to be universally fatal, the risk of dying with adequate and timely treatment is currently about 1-4%. Up to 1% of children with DKA develop complications known as cerebral edema. Between 2 and 5 out of 10 children who develop brain swelling will die as a result.
History
The first complete description of diabetic ketoacidosis is associated with Julius Dreschfeld, a German pathologist working in Manchester, England. In his description, which he gave in lecture 1886 at the Royal College of Physicians in London, he drew a report by Adolph Kussmaul as well as explaining the main ketone, acetoacetate and? -hydroxybutyrate, and their chemical determination. This condition was almost universally fatal until the discovery of insulin in the 1920s; in the 1930s, the mortality rate fell to 29 per cent, and by the 1950s that figure became less than 10 per cent. The brain edema entity due to DKA was described in 1936 by a team of doctors from Philadelphia.
A number of studies since the 1950s have focused on the ideal treatment for diabetic ketoacidosis. Much of this research has been done at the University of Tennessee Health Science Center and Emory University School of Medicine. Treatment options studied have included high or low intravenous, subcutaneous or intramuscular doses (eg "Alberti" insulin), phosphate supplementation, the need for insulin-loading doses, and the appropriateness of bicarbonate therapy in moderate DKA. Questions remain unanswered, such as whether bicarbonate administration in severe DKA makes a noticeable difference in clinical course, and whether insulin charge doses are required in adults.
Type 2 diabetes insulin vulnerable was first described fully in 1987 after several previous case reports. Initially regarded as a form of early-onset diabetes, and through several other descriptive names (such as "idiopathic type 1 diabetes", "Flatbush diabetes", "atypical diabetes" and "type 1.5 diabetes") before the current terminology of "type 2 diabetes ketosis vulnerable "was adopted.
References
External links
Source of the article : Wikipedia
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