C.Maintenance Water Needs.
= 100 mL/kg for first 10 kg of body weight
+ 50 mL/kg for next 10 kg
+ 20 mL/kg for weight greater than 20 kg

D.Clinical Signs of Hyponatremia. Confusion, agitation, lethargy, seizures, and coma. The rate of change of sodium concentration during onset of hyponatremia is more important in causing symptoms than is the absolute concentration of sodium.

1. A marked elevation of the blood glucose creates an osmotic gradient that pulls water from cells into the extracellular fluid, diluting the extracellular sodium. The contribution of hyperglycemia to hyponatremia can be estimated using the following formula:

The percentage of plasma water can be estimated with the following formula: % plasma water = 100 - [0.01 x lipids (mg/dL)] - [0.73 x protein (g/dL)]

Pseudohyponatremia should be excluded by repeat testing, then the cause of the hyponatremia should be determined based on history, physical exam, urine osmolality, and urine sodium level. An assessment of volume status should determine if the patient is volume contracted, normal volume, or volume expanded.

a.High urine sodium (>40 mEq/L) and volume contraction indicates a renal source of sodium and fluid loss (excessive diuretic use, salt-wasting nephropathy, Addison's disease, osmotic diuresis).

b.High urine sodium (>40 mEq/L) and normal volume is most likely caused by water retention due to a drug effect, hypothyroidism, or the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In SIADH, the urine sodium level is usually high, but may be low if the patient is on a salt-restricted diet. SIADH is found in the presence of a malignant tumor or a disorder of the pulmonary or central nervous system.

c.Low urine sodium (<20 mEq/L) and volume contraction, dry mucous membranes, decreased skin turgor, and orthostatic hypotension indicate an extrarenal source of fluid loss (gastrointestinal disease, burns).

d.Low urine sodium (<20 mEq/L) and volume-expansion, and edema is caused by congestive heart failure, cirrhosis with ascites, or nephrotic syndrome. Effective arterial blood volume is decreased. Decreased renal perfusion causes increased reabsorption of water.

restricted to 1,000 mL/day. Food alone in the diet contains this much water, so no liquids should be consumed. If an intravenous solution is needed, an isotonic solution of 0.9% sodium chloride (normal saline) should be used. Dextrose should not be used in the infusion because the dextrose is metabolized into water.

1. Ifneurologicsymptomsofhyponatremiaarepresent,theserumsodiumlevel should be corrected with hypertonic saline. Excessively rapid correction of sodium may result in a syndrome of central pontine demyelination.

hyponatremia has been chronic, the rate should be limited to 0.5 mEq/L per hour. The goal of initial therapy is a serum sodium of 125-130 mEq/L, then water restriction should be continued until the level normalizes.

4. Hypertonic 3% sodium chloride contains 513 mEq/L of sodium. The calculated volume required should be administered over the period required to raise the serum sodium level at a rate of 0.5-1 mEq/L per hour.

2. Clinical manifestations include tremulousness, irritability, ataxia, spasticity, mental confusion, seizures, and coma. Symptoms are more likely to occur with acute increases in plasma sodium.

2. Failure to replace obligate water losses may cause hypernatremia, as in patients unable to obtain water because of an altered mental status or severe debilitating disease.

1. If there is evidence of hemodynamic compromise (eg, orthostatic hypotension, marked oliguria), fluid deficits should be corrected initially with isotonic saline.