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Treatment of hyperglycemia in non diabetics,diabetes type 1 medical treatment review,slither browser - PDF Books

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.
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. 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. 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.
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 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. 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.
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.
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. Checking magnesium levels and correcting low levels should be considered in patients with DKA. 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.



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