Overly rapid treatment of hypernatremic dehydration maycause significant morbidity and mortality. Idiogenic osmolesare generated within the brain during the development ofhypernatremia. Idiogenic osmoles increase the osmolalitywithin the cells of the brain, providing protection againstbrain cell shrinkage secondary to movement of water out of cells into the hypertonic extracellular fluid. These idiogenicosmoles dissipate slowly during correction of hypernatremia.With rapid lowering of the extracellular osmolality duringcorrection of hypernatremia, a new gradient may be createdthat causes water movement from the extracellular spaceinto the cells of the brain, producing cerebral edema. Possible manifestations of the resultant cerebral edema include altered mental status, seizures, and potentially lethal brainherniation.
To minimize the risk of cerebral edema during correctionof hypernatremic dehydration, the serum sodium concentration should not decrease more than 12 mEq/L every 24 hours(Figure 33-1). The deficits in severe hypernatremic dehydration may need to be corrected over 2 to 4 days. The choice andrate of fluid are not nearly as important as vigilant monitoring of the serum sodium concentration and adjustment of thetherapy based on the result (see Figure 33-1). Nonetheless, theinitial resuscitation-rehydration phase of therapy remains thesame as for other types of dehydration.
Mild to moderate dehydration from diarrhea of any cause canbe treated effectively using a simple, oral rehydration solution (ORS) containing glucose and electrolytes (see Chapter112). The ORS relies on the coupled transport of sodium andglucose in the intestine. Oral rehydration therapy has significantly reduced the morbidity and mortality from acute diarrhea but is underused in developed countries. It should beattempted for most patients with mild to moderate diarrhealdehydration. Oral rehydration therapy is less expensive thanIV therapy and has a lower complication rate. IV therapymay still be required for patients with severe dehydration;patients with uncontrollable vomiting; patients unable todrink because of extreme fatigue, stupor, or coma; or patients with gastric or intestinal distention. Rapidly absorbed ondansetron may be used to treat vomiting, thus facilitating oralrehydration.
Restore intravascular volume: Normal saline: 20 mL/kg over 20 min (repeat until intravascular volume restored) Determine time for correction based on initial sodium concentration [Na] 145–157 mEq/L: 24hr [Na] 158–170 mEq/L: 48hr [Na] 171–183 mEq/L: 72hr [Na] 184–196 mEq/L: 84hr Administer fluid at a constant rate over the time for correction Typical fluid: D5 1/2 normal saline (with 20 mEq/L KCI unless contraindicated) Typical rate: 1.25–1.5 times maintenance Follow serum sodium concentration and adjust fluid based on clinical status and serum sodium concentration Signs of volume depletion Sodium decreases too rapidly Sodium decreases too slowly Replace excessive ongoing losses as they occur Decrease sodium concentration of IV fluid or increase rate of IV fluid Increase sodium concentration of IV fluid or decrease rate of IV fluid Administer normal saline (20 mL/kg)
Figure 33-1 Strategy for correcting hypernatremic dehydration.