MANAGEMENT OF DIABETIC KETOACIDOSIS: Because of the severe volume depletion that occurs as a result of hyperglycemia, isotonic fluids are given intravenously. As DKA reflects a state of insulin deficiency, IV insulin therapy is also administered. Finally, careful attention must be paid to electrolyte levels, with cautious addition of those ions whose levels have been depleted.
For example, potassium re-enters cells as the acidosis resolves and will also are driven into cells by insulin. This exit of potassium from the blood will unveil previously masked potassium depletion (from urine losses).
Life-threatening hypokalemia can occur, so there should be close monitoring and replacement. If infection is the precipitating cause of DKA, broad spectrum antibiotics should be administered (iRocket, 2005).
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 (Joint British Diabetes Societies Inpatient Care Group, 2010).
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 (Kitabchi et al., 2009).
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/1; if the level is any lower, administering insulin could lead to a dangerously low potassium level (Kitabchi et aL, 2009). 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; some recommend reducing the dose of insulin once glucose falls below 16.6 mmol/1 (300 mg/dl) (Kitabchi et al, 2009).
Potassium levels can fluctuate severely during the treatment of DKA, because insulin decreases potassium levels in the blood by redistributing it into cells. 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 (National Institute for Health and Clinical Excellence, 2004), as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids once levels fall below 5.3 mmol/1. If potassium levels fall below 3.3 mmol/1, insulin administration may need to be interrupted to allow correction of the hypokalemia (Kitabchi et al., 2009).
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 (Dunger et a.L, 2004).
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.