prevented in those known to have diabetes to an extent by adherence to "sick day rules"; these are clear-cut instructions to patients on how to treat themselves when unwell. instructions include advice on how much extra insulin to take when sugar levels appear uncontrolled, an easily digestible diet rich in salt and carbohydrates, means to suppress 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 are elevated. management 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 (icu) or similar high-dependency area or ward for close observation may be necessary. fluid replacement the amount of fluid replaced depends on the estimated degree of dehydration. if dehydration is so severe as to cause shock (severely decreased blood pressure with insufficient blood supply to the body's organs), or a depressed level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in repeated doses for children) is recommended to restore circulating volume. slower rehydration based on calculated water and sodium shortage may be possible if the dehydration is moderate, and again saline is the recommended fluid. very mild ketoacidosis with no associated vomiting and mild dehydration may be treated with oral rehydration and subcutaneous rather than intravenous insulin under observation for signs of deterioration. normal saline (0.9% saline) has generally been the fluid of choice. there have been a few small trials looking at balanced fluids with few differences. 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. 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 vein), and the administration of medication that increases the heart pumping action and blood pressure. insulin some guidelines recommend a bolus (initial large dose) of insulin of 0.1 unit of insulin per kilogram of body weight. this can be administered immediately after the potassium level is known to be higher than 3.3 mmol/l; if the level is any lower, administering insulin could lead to a dangerously low potassium level (see below). other guidelines recommend a bolus given intramuscularly if there is a delay in commencing an intravenous infusion of insulin, whereas guidelines for the management of pediatric dka recommend delaying the initiation of insulin until fluids have been administered. it is possible to use rapid acting insulin analogs injections under the skin for mild or moderate cases. in general, insulin is given at 0.1 unit/kg per hour to reduce the blood sugars and suppress ketone production. guidelines differ as to which dose to use when blood sugar levels start falling; american guidelines recommend reducing the dose of insulin once glucose falls below 16.6 mmol/l (300 mg/dl) and uk guidelines at 14 mmol/l (253 mg/dl). others recommend infusing glucose in addition to saline to allow for ongoing infusion of higher doses of insulin. potassium 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. a 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 5.3 mmol/l. if potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to allow correction of the hypokalemia. sodium bicarbonate the administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. 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. its use is therefore discouraged, although some guidelines recommend it for extreme acidosis (ph<6.9), and smaller amounts for severe acidosis (ph 6.9–7.0). cerebral edema cerebral edema, if associated with coma, often necessitates 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 established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling. cerebral edema is unusual in adults. resolution resolution of dka is defined as general improvement in the symptoms, such as the ability to tolerate oral nutrition and fluids, normalization of blood acidity (ph>7.3), and absence of ketones in blood (<1 mmol/l) or urine. 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 detected), or whether to withdraw insulin and attempt treatment with oral medication as in type 2 diabetes. generally speaking, routine measurement of c-peptide as a measure of insulin production is not recommended unless there is genuine doubt as to whether someone has type 1 or type 2 diabetes. epidemiology diabetic ketoacidosis occurs in 4.6–8.0 per 1000 people with diabetes annually. rates among those with type 1 diabetes are higher with about 4% in united kingdom developing dka a year while in malaysia the condition affects about 25% a year. in the united states, 135,000 hospital admissions occur annually as a result of dka, at an estimated cost of $2.4 billion or a quarter to a half the total cost of caring for people with type 1 diabetes. there has been a documented increasing trend to hospital admissions. the risk is increased in those with an ongoing risk factor, such as an eating disorder, and those who cannot afford insulin. about 30% of children with type 1 diabetes receive their diagnosis after an episode of dka. lower socio‐economic status and higher area‐level deprivation are associated with an increased risk of diabetic ketoacidosis in people with diabetes mellitus type 1. previously considered universally fatal, the risk of death with adequate and timely treatment is between <1% and 5%. up to 1% of children with dka develop a complication known as cerebral edema. rates of cerebral edema in us children with dka has risen from 0.4% in 2002 to 0.7% in 2012. between 2 and 5 out of 10 children who develop brain swelling will die as a result. history the first full description of diabetic ketoacidosis is attributed to julius dreschfeld, a german pathologist working in manchester, united kingdom. in his description, which he gave in an 1886 lecture at the royal college of physicians in london, he drew on reports by adolph kussmaul as well as describing the main ketones, acetoacetate and β-hydroxybutyrate, and their chemical determination. the condition remained almost universally fatal until the discovery of insulin in the 1920s; by the 1930s, mortality had fallen to 29 percent, and by the 1950s it had become less than 10 percent. the entity of cerebral edema due to dka was described in 1936 by a team of doctors from philadelphia. numerous research studies since the 1950s have focused on the ideal treatment for diabetic ketoacidosis. a significant proportion of these studies have been conducted at the university of tennessee health science center and emory university school of medicine. treatment options studied have included high- or low-dose intravenous, subcutaneous or intramuscular (e.g. the "alberti regime") insulin, phosphate supplementation, need for a loading dose of insulin, and appropriateness of using bicarbonate therapy in moderate dka. various questions remain unanswered, such as whether bicarbonate administration in severe dka makes any real difference to the clinical course, and whether an insulin loading dose is needed in adults. the entity of ketosis-prone type 2 diabetes was first fully described in 1987 after several preceding 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 1.5 diabetes") before the current terminology of "ketosis-prone type 2 diabetes" was adopted.