As hypernatremia develops, the brain generates idiogenic osmoles to increase the intracellular osmolality and prevent the loss of brain water. This mechanism is not instantaneous and is most prominent when hypernatremia has developed gradually. If the serum sodium concentration is lowered rapidly, there is movement of water from the serum into the brain cells to equalize the osmolality in the two compartments. The resultant brain swelling manifests as seizures or coma. Because of these dangers, corrected hypernatremia should be treated gradually. The goal is to decrease the serum sodium by less than 12 mEq/L every 24 hours (see Fig. 33-1). The most important component of correcting moderate or severe hypernatremia is frequent monitoring of the serum sodium to allow adjustment of fluid therapy and provide adequate correction that is neither too slow nor too fast.
In a child with hypernatremic dehydration, as in any childwith dehydration, the first priority is restoration of intra-vascular volume with isotonic fluid. Figure 33-1 outlines a general approach for correcting hypernatremic dehydrationsecondary to gastroenteritis. If the hypernatremia and dehydration are secondary to water loss, as occurs with diabetes insipidus, a more hypotonic IV fluid is appropriate. A child with central diabetes insipidus should receive an ADH analog to prevent further excessive water loss. A child withnephrogenic diabetes insipidus requires a urine replacementsolution to offset ongoing water losses. Chronically, reducedsodium intake, thiazide diuretics, and nonsteroidal anti-inflammatory drugs can decrease water losses in nephrogenic diabetes insipidus.
Acute, severe hypernatremia, usually secondary to sodium administration, can be corrected more rapidly because idiogenic osmoles have not had time to accumulate; this balances the high morbidity and mortality from severe, acute hypernatremia with the dangers of overly rapid correction. When hypernatremia is due to sodium intoxication, and the hypernatremia is severe, it may be impossible to administer enough water to correct the hypernatremia rapidly without worsening volume overload. Some patients require use of a loop diuretic or dialysis.
The kidneys are the principal regulator of potassium balance, adjusting excretion based on intake. Factors affecting renal potassium excretion include aldosterone, acid-base status, serum potassium concentration, and renal function. The intracellular potassium concentration is approximately 30 times the extracellular potassium concentration. A variety of conditions alter the distribution of potassium between the intracellular and extracellular compartments, potentially causing either hypokalemia or hyperkalemia. The plasma concentration does not always reflect the total body potassium content.
Available @ StudentConsult.com
Hypokalemia is common in children, with most cases related to gastroenteritis. Spurious hypokalemia occurs in patients with leukemia and elevated white blood cell counts if plasma for analysis is left at room temperature, permitting the white blood cells to take up potassium from the plasma. There are four basic mechanisms of hypokalemia (Table 36-1). Low intake, nonrenal losses, and renal losses all are associated with total body potassium depletion. With a transcellular shift, total body potassium is normal unless there is concomitant potassium depletion secondary to other factors.