Disorders of Water and Sodium Balance

I. Pathophysiology of Water and Sodium Balance

A. Volitional intake of water is regulated by thirst.
B. Maintenance intake of water is the amount of water sufficient to offset
obligatory losses.
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.
E. Pseudohyponatremia
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:
Expected change in serum sodium = (Serum glucose - 100) x 0.016
2. Marked elevation of plasma solids (lipids or protein) can also result in
erroneous hyponatremia because of laboratory inaccuracy. 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)]
II. Diagnostic Evaluation of Hyponatremia
A. 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.
B. Classification Hyponatremic Patients Based on Urine Osmolality
1. Low urine osmolality (50-180 mOsm/L) indicates primary excessive
water intake (psychogenic water drinking).
2. High Urine Osmolality (urine osmolality >serum osmolality)
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.
III. Treatment of Water Excess Hyponatremia
A. Determine the Volume of Water Excess
Water excess = total body water x [(140/measured sodium) -1]
B. Treatment of Asymptomatic Hyponatremia. Water intake should be
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.
C. Treatment of Symptomatic Hyponatremia
1. If neurologic symptoms of hyponatremia are present, the serum sodium level
should be corrected with hypertonic saline. Excessively rapid correction of
sodium may result in a syndrome of central pontine demyelination.
2. The serum sodium should be raised at a rate of 1 mEq/L per hour. If
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.
3. The amount of hypertonic saline needed is estimated using the following
formula:
Sodium needed (mEq) = 0.6 x wt in kg x (desired sodium - measured
sodium)
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.
5. Concomitant administration of furosemide may be required to lessen the risk
of fluid overload, especially in the elderly.
IV. Hypernatremia
A. Clinical Manifestations of Hypernatremia
1. Signs of either volume overload or volume depletion may be prominent.
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.
B. Causes of Hypernatremia
1. Net sodium gain or net water loss will cause hypernatremia
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.
3. Diabetes Insipidus: If urine volume is high but urine osmolality is low,
diabetes insipidus is the most likely cause.
V. Management of Hypernatremia
A. Acute treatment of hypovolemic hypernatremia depends on the degree of
volume depletion.
1. If there is evidence of hemodynamic compromise (eg, orthostatic
hypotension, marked oliguria), fluid deficits should be corrected initially with
isotonic saline.
2. Once hemodynamic stability is achieved, the remaining free water deficit
should be corrected with 5% dextrose water or 0.45% NaCl.
3. The water deficit can be estimated using the following formula:
Water deficit = 0.6 x wt in kg x [1 - (140/measured sodium)]
B. The change in sodium concentration should not exceed 1 mEq/liter/hour.
Roughly one half of the calculated water deficit can be administered in the first
24 hours, followed by correction of the remaining deficit over the next 1-2 days.
The serum sodium concentration and ECF volume status should be evaluated
every 6 hours. Excessively rapid correction of hypernatremia may lead to
lethargy and seizures secondary to cerebral edema.
C. Maintenance fluid needs from ongoing renal and insensible losses must also
be provided. If the patient is conscious and able to drink, water should be given
orally or by nasogastric tube.
VI. Mixed Disorders
A. Water excess and saline deficit occurs when severe vomiting and diarrhea
occur in a patient who is given only water. Clinical signs of volume contraction
and a low serum sodium are present. Saline deficit is replaced and free water
intake restricted until the serum sodium level has normalized.
B. Water and saline excess often occurs with heart failure with edema and a low
serum sodium. An increase in the extracellular fluid volume, as evidenced by
edema, is a saline excess. A marked excess of free water expands the
extracellular fluid volume, causing apparent hyponatremia. However, the
important derangement in edema is an excess of sodium. Sodium and water
restriction and use of diuretics (furosemide) are usually indicated in addition to
treatment of the underlying disorder.
C. Water and saline deficit is frequently caused by vomiting and high fever and
is characterized by signs of volume contraction and an elevated serum sodium.
Saline and free water should be replaced in addition to maintenance amounts
of water.