Osmotic pressure or Osmolality mOsmkg [Na mEqL K mEqL Glucose mgdl Urea mgdl

If increase in plasma osmolality is greater than 340mOsm/kg H2O, lethargy or coma is justified. Despite this, many people with lower osmolality values have clouding of sensorium, to which other factors seem to contribute as well: hyperketonaemia (alters brain oxygen consumption) and the frequently underlying disease (sepsis, etc.) are the most common.

The aims of therapy are:

1. Immediate priority: Rehydration - restoration of intravascular volume, aiming at restoring blood pressure, pulse rate and diuresis

2. Control of blood glucose (with insulin)

3. Replenishment of potassium losses

4. Correction of severe acidosis

First priority is replenishment of water deficit, since it can cause potentially dangerous hypovolaemia. Consequently, initial therapy should include the intravenous infusion of NaCI isotonic solution, at a rate of 1000 ml in the first hour (15-20 ml/kg/h). In hypovolaemic shock, this rate is continued further. Usually, another 1000 ml are infused in the following two hours (4-14ml/kg/h) and then 1000ml in four hours (4-14 ml/kg/h). If the patient is in hypovolaemic shock, an infusion of a colloidal solution or plasma will probably be needed. A total of 6-12 L of fluids may be needed in the first 24 hours.

Apart from fluids, insulin is infused, in the following way: initially a bolus injection of 10 IU regular insulin is given intravenously (0.15 IU/ kg), and an intravenous infusion of 5-10 IU/hr is started at the same time (12.5-25 ml/h of a solution containing 100 IU regular insulin in 250 ml NaCl). This rate is achieved by using the special pumps of intravenous fluid administration or with a microdroplet infusion system. Blood glucose is measured hourly and the infusion rate is promptly adjusted (desirable decrease of glucose by 50-70mg/dl/h [2.8-3.9mmol/L/h]). Thus, if blood glucose does not decrease by at least 50-70 mg/dl (2.8-3.9mmol/L) in one hour, the infusion rate should be doubled. When plasma glucose drops to 250 mg/dl (13.9 mmol/L), the infusion solution is converted to dextrose in water 5 percent (DW5 percent) at a rate of 150-250ml/h (+0.45 percent NaCl) with simultaneous continuous insulin iv infusion (2-4IU/h). Blood glucose target is 150-250 mg/dl (8.313.9 mmol/L), until metabolic control is stabilized.

It should be noted that although the various protocols of fluid and insulin infusion can vary in different hospitals, they are virtually similar regarding their basic principles and therapeutic targets.

For example, there are protocols that do not include a continuous insulin infusion, but only repeated bolus injections of insulin iv. Other protocols call for repeated administration of insulin, both intravenously and subcutaneously.

It should be emphasized that usually in DKA there is a significant shortage of potassium (as is the case with the other electrolytes as well), regardless of the initial serum potassium concentration. The causes of potassium shortage are as follows:

• Metabolic acidosis and decreased glycolysis result in exit of potassium from the cells and this can lead to hyperkalaemia (despite the fact that total potassium content of the body is low). A significant contributor to the exit of potassium from the cells is protein catabolism in the muscles, due to insulinopenia.

• Osmotic diuresis and secondary aldosteronism (hypovolaemia due to dehydration) lead to significant kaliuresis and potassium shortage.

• When there is hypokalaemia, the shortage is very large and usually prolonged vomiting or diuretic treatment is also involved.

Potassium shortage is usually large, and the initially high concentration in the blood, due to acidosis, can be misleading. Very soon, with volume restoration and insulin infusion, potassium concentration drops precipitously. For this reason, it is imperative to monitor K+ levels very closely and to administer adequate quantities promptly to replenish the low levels.

Thus, if serum K+ concentration is < 5.5 mEq/L, we do not add any potassium in the infusion fluids, but we recheck the level in two hours. If K+ concentration is 3.5-5.5 mEq/L, we add 20-30 mmol K+ in each L of fluids and if it is < 3.5 mEq/L, we add 40 mmol K+ in each L of fluids per hour, until K+ concentration is normalized. (Hypokalaemia can be directly dangerous for the life of the patient and should be given priority in its management.) As regards hyponatraemia in DKA, this is due to various reasons:

• osmotic shift of water in the extracellular space;

• loss of sodium in the urine as a result of osmotic diuresis and as an accompanying kation of the excreted ketone bodies;

• accompanying vomiting;

• decreased intake due to nausea and vomiting;

• factitious (due to an increase in triglycerides or glucose) corrected sodium is calculated by the formula: measured Na + [(glucose/18) — 5.6]/2.

Bicarbonate (HCO—) administration for management of acidosis is advised only when blood pH is < 7.0. When pH is between 6.9-7.0, 44 mmol HCO— is adequate (infused over 30 minutes) and when pH is < 6.9, 88 mmol HCO— is infused. When bicarbonate is administered, potassium needs are increased, and thus some authors suggest a separate additional potassium infusion.

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  • martina
    How much sodium to add in DW5% to become isotonic?
    8 years ago
  • fre-qalsi
    Why we add 20 meq/l ?
    7 years ago

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