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Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA. Diabetic ketoacidosis and insulin resistance with subcutaneous terbutaline infusion: a case report.
Type 2 diabetes can be due to increased peripheral resistance to insulin or to reduced secretion of insulin. DKA is caused by reduced insulin levels, decreased glucose use, and increased gluconeogenesis from elevated counter regulatory hormones, including catecholamines, glucagon, and cortisol. A flowchart for the management of DKA in children and adolescents from the ADA guideline is shown in Figure 2.3 A growing problem is the development of type 2 diabetes in obese children. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels. The beta-hydroxybutyrate level may not normalize during the first one to two days of treatment. Blood glucose should be evaluated every one to two hours until the patient is stable, and the blood urea nitrogen, serum creatinine, sodium, potassium, and bicarbonate levels should be monitored every two to six hours depending on the severity of DKA.3 Cardiac monitoring may be warranted for patients with significant electrolyte disturbances. Hyperchloremia is a common but transient finding that usually requires no special treatment.Cerebral edema is a rare but important complication of DKA.
Although DKA is less common in these patients than among those with type 1 diabetes, it does occur. Most patients with DKA will need lifetime insulin therapy after discharge from the hospital.
The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue.
Treatment also should be directed at the underlying cause of the DKA, including antibiotics for suspected or identified infection.
C-peptide levels may be helpful for determining the type of diabetes and guiding subsequent treatment. In one study10 of ketoacidosis, amylase was elevated in 21 percent and lipase in 29 percent of patients. Although it is important to monitor urinary output, urinary catheterization is not advised routinely.INPATIENT VS. Infection, insulin omission, and other problems that may have precipitated ketoacidosis should be treated. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol.Abdominal pain may be a symptom of ketoacidosis or part of the inciting cause of DKA, such as appendicitis or cholecystitis. If pancreatitis is suspected, contrast-enhanced computed tomography (CT) may be useful for diagnosis in selected patients. Patients typically improve mentally with initial treatment of DKA, but then suddenly worsen. Glucose is then stored as glycogen in liver and muscle.Insulin also inhibits the release of glucagon and so blocks fat being used as an energy source.

Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes.
If the patient has significant hypertriglyceridemia, it can falsely lower glucose and sodium measurements by dilution. Treatment of suspected cerebral edema should not be delayed for these tests to be completed. There are one million to three million islets of Langerhans (pancreatic islets) and beta cells constitute 60-80% of all the cells. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician.
In more severe cases, seizures, pupillary changes, and respiratory arrest with brain-stem herniation may occur.
Insulin is synthesised from the proinsulin precursor molecule by the action of proteolytic enzymes, known as prohormone convertases, as well as the exoprotease carboxypeptidase E. If dextrose is not given, further ketosis may occur.INSULINAn intravenous insulin drip is the current standard of care for diabetic ketoacidosis, primarily because of the more rapid onset of action. Studies29 comparing intravenous insulin with subcutaneous or intramuscular insulin have found a quicker decrease in glucose and ketone levels, but no improvement in morbidity and mortality. Although the bicarbonate level typically is low, it may be normal or high in patients with vomiting, diuretic use, or alkali ingestion. Lispro and aspart (NovoLog) insulin are more expensive and do not work faster than regular insulin when given intravenously. There are a family of four specialised transporter proteins that carry glucose across the membrane. There were no significant differences in outcomes between the aspart and intravenous insulin regimens. A similar study29 comparing subcutaneous lispro insulin in a medical ward with an intravenous insulin drip in the intensive care unit showed similar outcomes, except for a 40 percent reduction in cost for patients treated in the medical ward.
GLUT4 carries glucose into muscle and adipose tissue after the insulin receptor has been stimulated - see diagram above. If the patient is on an insulin pump, it should be stopped, and the patient should be switched to an intravenous infusion.31If an intravenous infusion pump is not available, insulin can be given intramuscularly. This treats insulin resistance.Sulfonylureas (gliclazide) bind to an ATP-dependent potassium channel on the cell membrane of pancreatic beta cells. This depolarisation opens voltage-gated calcium channels which leads to increased fusion of insulin granulae with the cell membrane, and increased secretion of (pro)insulin.Glitazones also treat insulin resistance. They bind to peroxisome proliferator-activated receptor gamma (a nuclear regulatory protein) which influences insulin-sensitive genes, which enhance production of mRNAs of insulin-dependent enzymes. Potassium should be started as soon as adequate urine output is confirmed and the potassium level is less than 5 mEq per L.3 Usually 20 to 30 mEq (20 to 30 mmol) of potassium is given for each liter of fluid replacement.
Because there are no studies on patients with a pH level below 6.9, giving bicarbonate as an isotonic solution still is recommended.

It should be remembered that there is a temporary increased risk of lactic acidosis in situations where increased tissue hypoxia occurs, e.g.
This is increased in older age groups, mild-to-moderate hepatic impairment, and renal impairment.
In addition to alterations in magnesium metabolism from DKA, many patients with diabetes have taken medications such as diuretics that also may lower magnesium levels.
Symptoms of magnesium deficiency are difficult to recognize and overlap with symptoms caused by deficiencies of calcium, potassium, and sodium. Paresthesias, tremor, carpopedal spasm, agitation, seizures, and cardiac dysrhythmias all are reported symptoms. The trials that have been done indicate that the incidence of hypoglycaemia is equivalent to that of the older sulphonylureas.18ThiazolidinedionesThiazolidinediones (TDZs) or 'glitazones' - pioglitazone19 is the only one currently licensed in the UK.
Checking magnesium levels and correcting low levels should be considered in patients with DKA. Its mechanism of action is still subject to debate but is thought to act in a similar manner to metformin, increasing hepatic sensitivity to insulin, and enhancing glucose clearance. Serum sodium is falsely lowered by 1.6 mEq for every 100 mg per dL increase in blood glucose. Hyponatremia needs to be corrected only when the sodium level is still low after adjusting for this effect.
They also slow the rate of absorption of nutrients into the bloodstream by reducing gastric emptying, and may directly reduce food intake.
Both are rapidly deactivated by dipeptydyl peptidase-4 (DPP4) GLP1 is not useful in diabetes treatment, as it has a very short half-life and must be given as a continuous subcutaneous (SC) injection. Inhibiting the enzyme that inactivates GLP1 is more successful and several oral DPP4 inhibitors are available for type 2 diabetes management, e.g. Updated 3rd November 2008, accessed 29 Dec 2009Klip A, Leiter LA; Cellular mechanism of action of metformin.
Updated September 2005, accessed 29 Dec 2009Landgraf R, Bilo HJ, Muller PG; A comparison of repaglinide and glibenclamide in the treatment of type 2 diabetic patients previously treated with sulphonylureas. Updated 24 Feb 2009, accessed 29 Dec 2009Wada K, Nakajima A, Katayama K, et al; Peroxisome proliferator-activated receptor gamma-mediated regulation of neural stem cell proliferation and differentiation.
Updated 10 November 2009, accessed 29 Dec 2009Sitagliptin, New Drug Evaluation No 45, Regional Drug and Therapeutic Centre, (Aug 2007)Summary of Product Characteristics (SPC) - Galvus® 50 mg tablets (vildagliptin), Novartis Pharmaceuticals UK Ltd, electronic Medicines Compendium.
Updated Aug 2009, accessed 29 Dec 2009Summary of Product Characteristics (SPC) - Byetta® (exenatide), (5 micrograms and 10 micrograms solution for injection, prefilled pens), Eli Lilly and Company Limited, electronic Medicines Compendium.

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