C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
175
Symptoms include apathy, lethargy, and headache,
which can progress to disorientation, confusion,
gross motor weakness, and depression of deep ten-
don reflexes. Seizures and coma occur when serum
sodium levels reach extremely low levels.
22
These severe
effects, which are caused by cerebral edema, may be
irreversible.
Treatment.
The treatment of hyponatremia is determined
by the underlying cause, severity, and timing of onset.
21–23
When hyponatremia is caused by water intoxication, lim-
iting water intake or discontinuing medications that con-
tribute to SIADH may be sufficient. The administration
of a saline solution orally or intravenously may be needed
when hyponatremia is caused by sodium deficiency.
Symptomatic hyponatremia (i.e., neurologic manifesta-
tions) may be treated with hypertonic saline solution and
a loop diuretic, such as furosemide, to increase water elim-
ination. This combination allows for correction of serum
sodium levels while ridding the body of excess water. The
vasopressin receptor antagonists (vaptans) may be used in
the treatment of euvolemic hyponatremia.
22,23
The treatment of severe hyponatremia varies
depending on the timing of the onset of the disorder.
Cells, particularly those in the brain, tend to defend
against changes in cell volume caused by changes in
ECF osmolality by increasing or decreasing their
concentration of organic osmotically active mol-
ecules (called
osmolytes
) that can’t cross the cell
membrane.
22,25
In the case of prolonged water intoxi-
cation (greater than 48 hours), brain cells reduce their
concentration of osmolytes as a means of preventing
an increase in cell volume.
22
It takes several days for
brain cells to restore the osmolytes lost during hypona-
tremia. Thus, treatment measures that produce rapid
changes in serum osmolality may cause a dramatic
decrease in brain cell volume. One of the reported
effects of rapid treatment of hyponatremia, called the
osmotic demyelination syndrome,
is characterized by
destruction of the myelin sheath of the axons passing
through the brain stem.
22,23,25
This syndrome can cause
serious neurologic injury and sometimes death. In per-
sons with acute-onset hyponatremia (i.e., onset within
48 hours), in whom cerebral adaptation has not had
time to occur, rapid correction is less likely to result in
osmotic demyelination.
Hypernatremia
Hypernatremia is characterized by a serum sodium level
above 145 mEq/L (145 mmol/L) and a serum osmolal-
ity greater than 295 mOsm/kg H
2
O.
3
Because sodium
and its attendant anion is functionally an impermeable
solute, hypernatremia increases ECF tonicity, causing
movement of water out of the ICF, resulting in cellular
dehydration.
3,26–28
As with hyponatremia, hypernatremia can present
as an
euvolemic state,
in which water from the ICF is
TABLE 8-4
Manifestations of Hyponatremia and Hypernatremia
Hyponatremia
Hypernatremia
LaboratoryValues
LaboratoryValues
Serum sodium <135 mEq/L (135 mmol/L)
Serum sodium >145 mEq/L (145 mmol/L)
Decreased serum osmolality
Increased serum osmolality
Dilutional decrease in blood components, including
hematocrit, blood urea nitrogen (BUN)
Increased concentrations of blood components, including
hematocrit, BUN
Compensatory Mechanisms
Increased thirst
Increased ADH with oliguria and high urine specific gravity
Decreased Intracellular Fluid
Dry skin and mucous membranes
Decreased tissue turgor
Decreased salivation and lacrimation
Elevated body temperature
Hypo-osmolality and Movement ofWater into
Muscle and Neural Tissue
Muscle cramps and weakness
Depressed deep tendon reflexes
Headache
Disorientation
Lethargy
Seizures and coma (severe hyponatremia)
Gastrointestinal Tract
Anorexia, nausea, vomiting
Abdominal cramps, diarrhea
Hyperosmolality and Movement ofWater
out of Neural Tissue
Headache
Disorientation and agitation
Decreased reflexes
Seizures and coma (severe hypernatremia)
ADH, antidiuretic hormone.
