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From Emory University School of Medicine, Atlanta, Georgia, and University of Tennessee Health Science Center, Memphis, Tennessee.
Grant Support: In part by research grants from the American Diabetes Association (7-03-CR-35) (Dr. Several investigators have reported that more than half of African-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic features of type 2 diabetes during follow-up.
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Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in people with diabetes mellitus.
DKA may be the first symptom of previously undiagnosed diabetes, but it may also occur in people known to have diabetes as a result of a variety of causes, such as intercurrent illness or poor compliance with insulin therapy. The symptoms of an episode of diabetic ketoacidosis usually evolve over the period of about 24 hours. On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. Small children with DKA are relatively prone to cerebral edema (swelling of the brain tissue), which may cause headache, coma, loss of the pupillary light reflex, and progress to death.
DKA most frequently occurs in those who already have diabetes, but it may also be the first presentation in someone who had not previously been known to be diabetic.
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.g. Drugs in the gliflozin class (SGLT2 inhibitors), which are generally used for type 2 diabetes, have been associated with diabetic ketoacidosis with remarkably low blood sugars ("euglycemic DKA"). In various situations such as infection, insulin demands rise but are not matched by the failing pancreas. I?-hydroxybutyrate, despite chemically containing a carboxylic acid instead of a ketone, is the principal "ketone body" in diabetic ketoacidosis. 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.
Cerebral edema, which is the most dangerous DKA complication, is probably the result of a number of factors. Arterial blood gas measurement is usually performed to demonstrate the acidosis; this requires taking a blood sample from an artery. In addition to the above, blood samples are usually taken to measure urea and creatinine (measures of kidney function, which may be impaired in DKA as a result of dehydration) and electrolytes.

Diabetic ketoacidosis is distinguished from other diabetic emergencies by the presence of large amounts of ketones in blood and urine, and marked metabolic acidosis.
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. 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. A special but unusual consideration is cardiogenic shock, where the blood pressure is decreased not due to dehydration but due to inability of the heart to pump blood through the blood vessels.
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.
The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The first full description of diabetic ketoacidosis is attributed to Julius Dreschfeld, a German pathologist working in Manchester, United Kingdom. Numerous research studies since the 1950s have focused on the ideal treatment for diabetic ketoacidosis. The entity of ketosis-prone type 2 diabetes was first fully described in 1987 after several preceding case reports. Kitabchi: University of Tennessee Health Science Center, Room 334D, 956 Court Avenue, Memphis, TN 38163. These patients are usually obese, have a strong family history of diabetes, have a low prevalence of autoimmune markers, and lack a genetic association with HLA. One month after publication, editors review all posted comments and select some for publication in the Letters section of the print version of Annals. It is manifested by the sudden onset of severe hyperglycemia, rapid progression to diabetic ketoacidosis, and death unless treated with insulin.
Vomiting, dehydration, deep gasping breathing, confusion and occasionally coma are typical symptoms. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe.
If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. 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. 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.
Subsequent measurements (to ensure treatment is effective), may be taken from a normal blood test taken from a vein, as there is little difference between the arterial and the venous pH.[6] Ketones can be measured in the urine (acetoacetate) and blood (I?-hydroxybutyrate).

Furthermore, markers of infection (complete blood count, C-reactive protein) and acute pancreatitis (amylase and lipase) may be measured. It may also result from alcohol excess and from starvation; in both states the glucose level is normal or low.
A large part of the shifted extracellular potassium would have been lost in urine because of osmotic diuresis. There is little evidence that it improves outcomes beyond standard 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. Their initial presentation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating cause of metabolic decompensation. Acute insulin response to glucagon is the incremental change in C-peptide level over the baseline level. DKA is diagnosed with blood and urine tests; it is distinguished from other, rarer forms of ketoacidosis by the presence of high blood sugar levels. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. 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.[1] This leads to polyuria, dehydration, and compensatory thirst and polydipsia. At presentation, they have markedly impaired insulin secretion and insulin action, but intensified diabetic management results in significant improvement in I?-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of follow-up. The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis), which are converted through a process called beta oxidation, again in the liver, into ketone bodies (acetoacetate and I?-hydroxybutyrate). On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. I?-Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation.
The absence of autoimmune markers and the presence of measurable insulin secretion have proven useful in predicting near-normoglycemic remission and long-term insulin dependence in adult patients with a history of diabetic ketoacidosis.
The ketone bodies, however, have a low pKa and therefore turn the blood acidic (metabolic acidosis). This clinical presentation is commonly reported in African and African-American persons but is also observed in Hispanic persons and those from other minority ethnic groups.
The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and other mechanisms must work to compensate for the acidosis.[1] One such mechanism is hyperventilation to lower the blood carbon dioxide levels (a form of compensatory respiratory alkalosis).
The underlying mechanisms for I?-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, preliminary evidence suggests an increased susceptibility to glucose desensitization.

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