Replacement Fluid Therapy

The initial goal of treating dehydration is to restore intravascular volume (resuscitative phase). The simplest approach is to replace dehydration losses with 0.9% saline. This ensures that the administered fluid remains in the extracellular (intravascular) compartment, where it will do the most good to support blood pressure and peripheral perfusion.

Therapy may be started with a rapid bolus of 0.9% saline to combat incipient shock. But correction of dehydration must be accompanied by provision of maintenance fluid. After all, the child is breathing, losing free water through the skin, and is urinating! As discussed earlier, maintenance fluid is provided as D5NS.

A typical sequence of events in the management of a child with 10% dehydration AND A NORMAL SERUM SODIUM LEVEL is given below. Management of children with a serum sodium level of < 135 or> 145 mEq/L is beyond the scope of this discussion.

Step 1: In the ER, the child is estimated as having 10% dehydration. The blood pressure is low and the heart rate is very high. This child is in shock. The goal is to rapidly stabilize the vital signs; maintenance fluid is not a consideration at this time.

The child is given a 20 ml/kg bolus of 0.9% saline over 10-20 minutes. The vital signs stabilize (the bolus can be repeated if necessary).

Step 2: The patient is transferred to the inpatient unit. By this time, serum electrolyte levels are available and the serum sodium concentration is within the normal range. Subsequent fluid therapy is calculated as follows:

This child's total fluid loss was 10% of 10 kg, or 1000 ml. Of this, 200 ml has already been infused in the ER, so the remaining deficit is 800 ml.

Typically, half the total deficit is replaced in the first eight hours after admission and the remaining fluid is given over the next 16 hours. So, this child needs 300 ml of NS in the next eight hours (for a total of 500 ml) and another 500 ml in the next 16 hours.

However, maintenance fluid must also be administered. The volume of maintenance fluid for 24 hours is 1000 ml (100 ml/kg X 10 kg). This needs to be given as D5NS, with our without potassium, depending on the patient's urine output. If the child is not urinating well, hold on adding potassium.

Note #1: Once the child has started urinating, KCl should be added to the intravenous fluids at a concentration of 20 mEq/L.

Note #2: If the child continues to vomit or have significant diarrhea, the volume of ongoing fluid loss should be estimated and added to the deficit every few hours as 0.9% saline. Ideally, the diapers should be weighed. If this is not possible, then a volume of 50-100 ml should be used for each stool in an infant and 100-200 ml for the older child.

Note #3: The dehydration component of fluid replacement MUST be provided as 0.9% saline. NEVER use a hypotonic saline, such as D5 0.18% (fifth-normal saline), D5 0.3% (third-normal saline) or even D5 0.45% (half-normal saline) to correct dehydration. Dehydration and hypovolemia result in secretion of anti-diuretic hormone, which causes retention of free water, and provision of hypotonic replacement fluid can lead to potentially life-threatening hyponatremia.

Step 3: Suppose the child is well hydrated by the second hospital day, but is still feeling queasy and does not want to drink. Maintenance fluids can now be continued as D5 NS with 20 mEq/L of KCl.


  1. If you are correcting only dehydration (as when giving a bolus in the ER), use 0.9% saline.
  2. If you are providing fluid only, may use D5NS with 20 mEq/L KCl.
  3. Estimate and replace ongoing losses, if significant.

More info: hypernatremia and hyponatremia

The blood brain barrier prevents rapid movement of solutes out of or into the brain. On the other hand, water can move freely across the blood brain barrier. Rapidly developing hyponatremia causes a shift of water into the brain; conversely, hypernatremia can lead to brain dehydration and shrinkage.

Severe, acute hyponatremia may result in brain edema with neurological symptoms such as a change in sensorium, seizures, and respiratory arrest. This is a life-threatening medical emergency and requires infusion of hypertonic saline.

Acute hypernatremia results in a reduction in brain volume. This can lead to subdural bleeding from stretching and rupture of the bridging veins that extend from the dura to the surface of the brain.

Given time, the brain can alter intracellular osmotic pressure to better match plasma osmolality.

With persistent or slowly developing hyponatremia, brain cells extrude electrolytes and organic osmoles and the increase in brain volume is blunted or avoided. Neurologic symptoms are absent or subtle.

With persistent hypernatremia, brain cells generate organic osmoles (also known as idiogenic osmoles) to compensate for the increase in plasma osmolality. Again, the change in brain volume is partially blunted. These processes take 24-48 hours to become effective and leave the brain with a decreased (in hyponatremia) or increased (hypernatremia) osmolar content.

Just as the adaptation takes 24 hours or more, un-adaptation also takes time. Rapid correction of long-standing hypo- or hypernatremia has the potential for severe neurological consequences because of sudden changes in brain volume in the opposite direction. The neurologic manifestations associated with overly rapid correction of hyponatremia is called osmotic demyelination syndrome.

Thus, hyper- or hyponatremia of long duration should be corrected slowly.




Photo by Javier Correa from Photospin