DEFINITION
Hypernatremia, defined as a plasma sodium concentration greater than
144 mmol/L, always reflects a state of hypertonicity, with an increase in the
ratio of the concentration of osmotically active solutes to water throughout
all body fluid compartments because sodium is an osmotically effective ECF
solute.
EPIDEMIOLOGY AND PATHOBIOLOGY
Hypernatremic patients have undergone a process whereby water has moved
from the ICF to the ECF compartment,
accompanied by a reduction in ICF
volume and cell shrinkage. Cell shrinkage in the brain is associated with
intracerebral hemorrhage, which often punctates but sometimes disrupts
blood vessels, particularly at the brain surface and arachnoid interface. In an
effort to restore their cell volume, brain cells undergo osmotic adaptation by
accumulating sodium and other electrolytes and then subsequently producing
nonelectrolyte small solutes (osmolytes) such as inositol, taurine, glutamine,
and glutamate, among others. This process partially reverses cell
shrinkage, but at the price of an altered intercellular solute composition with
consequent perturbations in neuronal function.
Hypernatremia is the most frequent but not the only hypertonicity state
in clinical medicine. Glucose, mannitol, and glycerol can produce hypertonicity
states that may not be accompanied by hypernatremia and, in fact, are
frequently accompanied by hyponatremia (see earlier). In hypertonicity
states, the measured plasma osmolality is always high, but the converse is not
necessarily true because a number of solutes that contribute to the measured
plasma osmolality are not osmotically effective in terms of movement of
water from the ICF to the ECF compartment. Thus, patients with high concentrations
of urea or small alcohols (e.g., methanol, ethylene glycol, ethanol)
often have elevated plasma osmolality but should not be considered to have
a hypertonicity state.Although hypernatremia can be diagnosed as an incidental laboratory abnormality, it most commonly occurs in the setting of a severe underlying
disease with other accompanying disturbances in body fluid homeostasis.
In hypervolemic hypernatremia, a disproportionate excess of sodium as
opposed to water expands ECF volume, but ICF volume is decreased because
cells shrink. Hypervolemic hypernatremia usually occurs in the hospital
setting because inadvertent or overzealous administration of hypertonic
saline, the administration of hypertonic sodium bicarbonate solutions during
cardiopulmonary resuscitation, or dialysis against a hypertonic dialysate can
lead to hypervolemic hypernatremia in the clinical setting.
In normovolemic hypernatremia, a pure water deficit with no disturbance in
body sodium content does not generally result in a clinically perceptible
decrease in ECF volume because the predominant (approximately two
thirds) origin of the water deficit is in the ICF rather than the ECF compartment.
Thus, for example, a 3-L pure net water deficit will reduce ECF volume
by only 1 L, approximately 300 mL of which emanates from plasma water.
Yet a 3-L or greater deficit certainly increases body fluid tonicity and the
measured plasma sodium concentration. Therefore, such pure net water deficits
with no change in body sodium content often are considered to be
approximately normovolemic. Clinical conditions that fit this category
require a source of fluid loss that has a relatively low content of osmotically
effective solutes (principally sodium and potassium and their accompanying
anions), such as the various forms of diabetes insipidus or use of vaptan drugs
without adequate monitoring. In these conditions, profuse volumes of low
osmolality urine are excreted. However, hypernatremia is actually uncommon
as long as thirst perception and availability of water remain intact. The
principal clinical manifestation is polyuria and polydipsia (see later). Insensible
evaporative losses from the skin and respiratory tract also are a source
of hypotonic fluid loss. Increased fluid loss can occur in febrile patients (skin
and respiratory tract), patients on mechanical ventilation (respiratory tract),
and patients with profuse sweating. The sweat sodium concentration
decreases with increasing volumes of perspiration. These conditions will lead
to hypernatremia with body fluid hypertonicity only if the thirst mechanism
or access to water is impaired.
Hypovolemic hypernatremia is by far the most common hypertonicity state.
Patients with hypovolemic hypernatremia have lost both sodium and water,
but the net loss of water is disproportionately greater than the net loss of
sodium. The actual plasma sodium concentration resulting from loss of hypotonic
fluid depends not only on the sodium concentration of the fluid lost
but also on the concentration of other osmotically active solutes, such as
potassium, and on the solute composition of concomitantly ingested or
administered fluids. The extrarenal and renal causes of such fluid losses are
similar to those of hypovolemia. Among gastrointestinal causes of hypovolemic
hypernatremia, diarrhea is more common than vomiting, and osmotic
diarrheas result in disproportionately greater loss of water than electrolytes,
with a greater propensity to hypernatremia than for secretory diarrheas.
Among the renal sources of sodium and water loss, the two most common
causes are loop natriuretic medications and osmotic diuresis. Loop natriuretic
agents interfere with the countercurrent mechanism and generate large
volumes of urine with an iso-osmolar composition. Because some of the
solutes are nonelectrolyte (urea), the impact on body tonicity may be to
increase tonicity, unless there is concomitant intake or administration of
hypotonic fluids. In contrast, thiazides do not interfere with the countercurrent
mechanism and therefore rarely promote hypernatremia. The presence
of nonelectrolyte solutes in urine causes an osmotic diuresis. Such solutes can
be of either endogenous origin (e.g., urea or glucose) or exogenous origin
(e.g., mannitol or glycerol). The presence of these solutes in tubular fluid
impairs both sodium and water reabsorption, but the excretion of urine
that is relatively rich in nonelectrolyte solutes tends to promote body fluid
hypertonicity, unless sufficient hypotonic fluids are ingested or administered
concomitantly.
Failure to replace hypotonic fluid losses generally reflects either impairment
in thirst, disability, or infirmity that prevents the patient from responding
to thirst, or failure of the clinician to recognize the need for hypotonic
fluid replacement. Rarely, impaired thirst in patients who are awake and alert
can be caused by damage to the hypothalamic osmoreceptors that control
thirst perception and response, a condition known as primary hypodipsia.
Usually this condition tends to be associated with an abnormality in the
osmotic regulation of AVP secretion. However, cases have been described in
which the osmotic regulation of AVP secretion has been dissociated from the
osmotic regulation of thirst. Such patients suffer hypernatremia only when
extrarenal fluid losses exceed their habitual water intake, as might occur in
settings of thermal stress or exercise.
CLINICAL MANIFESTATIONS
The clinical features of patients with hypernatremia can be divided into those
associated with the underlying disease state, those associated with a concomitant
disturbance in ECF volume, and those associated with an increase in
body fluid tonicity. The main clinically relevant consequence of increased
body fluid tonicity is decreased brain cell volume, with the attendant risk for
intracerebral hemorrhage. Thus, the major symptoms are neurologic and
include confusion, seizures, focal neurologic deficits, and a progressively
decreasing level of consciousness that can progress to coma. In the absence
of an underlying neurologic problem or disturbance in the thirst mechanism,
the patient would be expected to complain of thirst unless the neurologic
injury has disturbed consciousness.
In patients with hypernatremia of sufficient duration to enable brain cells
to undergo osmotic adaptation, the risk for intracerebral hemorrhage from
cell shrinkage is decreased, but a hypertonic intracellular environment with
the accumulation of new intracellular solutes can perturb normal cellular
function.
DIAGNOSIS:
The diagnosis of hypernatremia is made by laboratory testing of the sodium
concentration, which always should be repeated to confirm its accuracy, corroborated
by measurement of plasma osmolality, which is expected to be
elevated in all cases. The underlying cause of the hypernatremia is usually
evident from the history and physical examination. The history should
include a review of recent and current medication use and questions regarding
exercise, heat exposure, sweating, vomiting, diarrhea, urine output, recent
fluid intake, and the presence of thirst. Physical examination should include
an assessment of ECF volume and a complete neurologic evaluation. Urine
volume should be monitored, urine osmolality should be measured in several
spot urine samples, and 24-hour urine osmolar excretion should be measured
if polyuria is present. In the less common situation of hypervolemic
hypernatremia, there is often an antecedent history of the administration of
sodium-containing solutions, and the findings on physical examination are
consistent with ECF volume expansion. In the absence of underlying intrinsic
renal disease or diuretic action, urine osmolality should be high because
of the hypertonic stimulus to AVP release, which overrides the attenuating
effect of hypervolemia. In such patients, the urine sodium concentration
should be elevated in response to hypervolemia.
In the more common condition of hypovolemic hypernatremia with extrarenal
fluid loss, urine output should be reduced to less than 500 mL/day, and
urine osmolality should be the maximum expected for age (urine osmolality
>1000 mOsm/kg in young adulthood and decreasing to >600 mOsm/kg by
the seventh decade of life and beyond). Polyuria with a submaximal urine
osmolality in the presence of hypernatremia suggests impaired urine-concentrating
ability, such as occurs with preexisting or underlying intrinsic renal
disease or exposure to diuretic agents. A spot urine osmolality measurement
less than 100 to 200 mOsm/kg or polyuria (>3 L/day), together with
24-hour urine solute excretion less than 600 mOsm/day in the face of hypernatremia,
suggests diabetes insipidus. In contrast, daily solute excretion
exceeding 800 to 1000 mOsm/day suggests an osmotic diuresis, which can
be confirmed by measuring glucose and urea in urine.
TREATMENT:
The main components of treatment are to treat the underlying disorder,
correct the abnormality in ECF volume, replace the water deficit, and provide
maintenance fluids to match continuing ongoing fluid losses if they persist.
The therapeutic approach to serious symptomatic hypovolemic hypernatremia
is challenging and often controversial. It is best to divide the therapeutic
approach into two separate phases: rapid correction of the depleted ECF
volume, followed by gradual replacement of the water deficit, including provision
for ongoing fluid losses. When ECF volume contraction is severe, as evidenced
by tissue hypoperfusion and shock, administered fluid should have a
sodium concentration as close as possible to that of the patient and should
distribute to the ECF or even the intravascular compartment. Isotonic saline is
generally the fluid of choice, and the volume and rate of administration should
be guided by clinical parameters related to reversal of hypovolemia. After the
patient’s tissue perfusion has been restored, further fluid replacement should
be aimed at correcting the estimated water deficit. This estimate begins with
a simple calculation of the percent deficit based on the measured sodium
concentration:
Total body water deficit premorbid = 0.6 × weight ×(1−[140/Na+ ])
Total body water is used because the sodium concentration reflects tonicity
in all body fluid compartments, including the ICF. Unlike the isotonic fluid
replacement for ECF volume, the water replacement should be administered
gradually over a period of hours to days, unless there is clear documentation
that the hypernatremia has itself evolved over minutes to hours. The necessity
for gradual replacement is dictated by the process of osmotic adaptation
described previously, and ideally, the rate of water replacement should match
the rate at which brain intracellular solutes can be adaptively extruded or
removed. More rapid rates of administration could result in brain cell swelling
with attendant dangerous neurologic consequences. It is recommended that
the estimated volume of the water deficit be replaced at a rate that will lead
to an approximately 0.5 to 1.0 mmol/L reduction in measured plasma sodium
concentration per hour. In addition to the estimated water deficit, the estimated
ongoing water loss during replacement should include at least 1 L per
24 hours of insensible fluid losses (greater volumes in patients who are febrile
or mechanically ventilated), supplemented with any ongoing water losses
(renal or gastrointestinal) resulting from continuation of the underlying
disease process. Because of the need to distribute replacement of the initial
water deficit, which can amount to several liters over a number of days during
which ongoing water losses continue, it is not unusual for patients to require
large volumes of water, sometimes reaching 5 to 10 L, over the duration of the
correction period. This water deficit, together with ongoing losses, can be
replaced by the dietary ingestion of tap water if the patient’s condition is suitable
or by an enteral feeding tube. If a gastrointestinal or other disease process
precludes these preferred routes, a hypotonic intravenous solution such as
D5W or half-normal saline can be used. When D5W is used, the glucose is either
stored as glycogen or fat or metabolized into carbon dioxide and water, thus
effectively providing the patient with solute-free water replacement. In the
case of half-normal saline, for any given liter administered, only half can be
considered as replacement of the water deficit, and the sodium content will
either replace any remaining sodium deficit that has not been fully corrected
in the first phase of treatment or be excreted if there is no impairment in
urinary sodium excretion. In elderly patients with known or possible underlying
cardiac, hepatic, or renal disease, caution should be exercised in the provision
of excessive volumes of salt-containing solutions. In any case, the sodium
concentration should be monitored at regular intervals of no less than every
4 hours to avoid too slow or too rapid correction, and ECF volume parameters
should be monitored to avoid hypervolemic complications.
Special considerations apply for hypertonic states in the setting of uncontrolled
diabetes with hyperglycemia (Chapters 236 and 237). The unusual cases
of patients with hypervolemic hypernatremia in the hospital setting also need
special attention and sometimes require continuous infusions of loop diuretics
together with the administration of hypotonic solutions or, in some cases,
extracorporeal means to remove both the sodium and water excess in a controlled
and safe manner under careful monitoring, often in the intensive care
unit.
The route of administration should change in accordance with the patient’s
response. Although an initial parenteral or nasogastric enteral route might be
appropriate when the patient’s neurologic status is compromised, subsequent
therapy can consist of simple dietary intake of water. Once a patient is awake
and alert and if thirst mechanisms are intact, the patient will generally correct
the hypertonic state by spontaneous oral fluid intake.
Hypernatremia, defined as a plasma sodium concentration greater than
144 mmol/L, always reflects a state of hypertonicity, with an increase in the
ratio of the concentration of osmotically active solutes to water throughout
all body fluid compartments because sodium is an osmotically effective ECF
solute.
EPIDEMIOLOGY AND PATHOBIOLOGY
Hypernatremic patients have undergone a process whereby water has moved
from the ICF to the ECF compartment,
accompanied by a reduction in ICF
volume and cell shrinkage. Cell shrinkage in the brain is associated with
intracerebral hemorrhage, which often punctates but sometimes disrupts
blood vessels, particularly at the brain surface and arachnoid interface. In an
effort to restore their cell volume, brain cells undergo osmotic adaptation by
accumulating sodium and other electrolytes and then subsequently producing
nonelectrolyte small solutes (osmolytes) such as inositol, taurine, glutamine,
and glutamate, among others. This process partially reverses cell
shrinkage, but at the price of an altered intercellular solute composition with
consequent perturbations in neuronal function.
Hypernatremia is the most frequent but not the only hypertonicity state
in clinical medicine. Glucose, mannitol, and glycerol can produce hypertonicity
states that may not be accompanied by hypernatremia and, in fact, are
frequently accompanied by hyponatremia (see earlier). In hypertonicity
states, the measured plasma osmolality is always high, but the converse is not
necessarily true because a number of solutes that contribute to the measured
plasma osmolality are not osmotically effective in terms of movement of
water from the ICF to the ECF compartment. Thus, patients with high concentrations
of urea or small alcohols (e.g., methanol, ethylene glycol, ethanol)
often have elevated plasma osmolality but should not be considered to have
a hypertonicity state.Although hypernatremia can be diagnosed as an incidental laboratory abnormality, it most commonly occurs in the setting of a severe underlying
disease with other accompanying disturbances in body fluid homeostasis.
In hypervolemic hypernatremia, a disproportionate excess of sodium as
opposed to water expands ECF volume, but ICF volume is decreased because
cells shrink. Hypervolemic hypernatremia usually occurs in the hospital
setting because inadvertent or overzealous administration of hypertonic
saline, the administration of hypertonic sodium bicarbonate solutions during
cardiopulmonary resuscitation, or dialysis against a hypertonic dialysate can
lead to hypervolemic hypernatremia in the clinical setting.
In normovolemic hypernatremia, a pure water deficit with no disturbance in
body sodium content does not generally result in a clinically perceptible
decrease in ECF volume because the predominant (approximately two
thirds) origin of the water deficit is in the ICF rather than the ECF compartment.
Thus, for example, a 3-L pure net water deficit will reduce ECF volume
by only 1 L, approximately 300 mL of which emanates from plasma water.
Yet a 3-L or greater deficit certainly increases body fluid tonicity and the
measured plasma sodium concentration. Therefore, such pure net water deficits
with no change in body sodium content often are considered to be
approximately normovolemic. Clinical conditions that fit this category
require a source of fluid loss that has a relatively low content of osmotically
effective solutes (principally sodium and potassium and their accompanying
anions), such as the various forms of diabetes insipidus or use of vaptan drugs
without adequate monitoring. In these conditions, profuse volumes of low
osmolality urine are excreted. However, hypernatremia is actually uncommon
as long as thirst perception and availability of water remain intact. The
principal clinical manifestation is polyuria and polydipsia (see later). Insensible
evaporative losses from the skin and respiratory tract also are a source
of hypotonic fluid loss. Increased fluid loss can occur in febrile patients (skin
and respiratory tract), patients on mechanical ventilation (respiratory tract),
and patients with profuse sweating. The sweat sodium concentration
decreases with increasing volumes of perspiration. These conditions will lead
to hypernatremia with body fluid hypertonicity only if the thirst mechanism
or access to water is impaired.
Hypovolemic hypernatremia is by far the most common hypertonicity state.
Patients with hypovolemic hypernatremia have lost both sodium and water,
but the net loss of water is disproportionately greater than the net loss of
sodium. The actual plasma sodium concentration resulting from loss of hypotonic
fluid depends not only on the sodium concentration of the fluid lost
but also on the concentration of other osmotically active solutes, such as
potassium, and on the solute composition of concomitantly ingested or
administered fluids. The extrarenal and renal causes of such fluid losses are
similar to those of hypovolemia. Among gastrointestinal causes of hypovolemic
hypernatremia, diarrhea is more common than vomiting, and osmotic
diarrheas result in disproportionately greater loss of water than electrolytes,
with a greater propensity to hypernatremia than for secretory diarrheas.
Among the renal sources of sodium and water loss, the two most common
causes are loop natriuretic medications and osmotic diuresis. Loop natriuretic
agents interfere with the countercurrent mechanism and generate large
volumes of urine with an iso-osmolar composition. Because some of the
solutes are nonelectrolyte (urea), the impact on body tonicity may be to
increase tonicity, unless there is concomitant intake or administration of
hypotonic fluids. In contrast, thiazides do not interfere with the countercurrent
mechanism and therefore rarely promote hypernatremia. The presence
of nonelectrolyte solutes in urine causes an osmotic diuresis. Such solutes can
be of either endogenous origin (e.g., urea or glucose) or exogenous origin
(e.g., mannitol or glycerol). The presence of these solutes in tubular fluid
impairs both sodium and water reabsorption, but the excretion of urine
that is relatively rich in nonelectrolyte solutes tends to promote body fluid
hypertonicity, unless sufficient hypotonic fluids are ingested or administered
concomitantly.
Failure to replace hypotonic fluid losses generally reflects either impairment
in thirst, disability, or infirmity that prevents the patient from responding
to thirst, or failure of the clinician to recognize the need for hypotonic
fluid replacement. Rarely, impaired thirst in patients who are awake and alert
can be caused by damage to the hypothalamic osmoreceptors that control
thirst perception and response, a condition known as primary hypodipsia.
Usually this condition tends to be associated with an abnormality in the
osmotic regulation of AVP secretion. However, cases have been described in
which the osmotic regulation of AVP secretion has been dissociated from the
osmotic regulation of thirst. Such patients suffer hypernatremia only when
extrarenal fluid losses exceed their habitual water intake, as might occur in
settings of thermal stress or exercise.
CLINICAL MANIFESTATIONS
The clinical features of patients with hypernatremia can be divided into those
associated with the underlying disease state, those associated with a concomitant
disturbance in ECF volume, and those associated with an increase in
body fluid tonicity. The main clinically relevant consequence of increased
body fluid tonicity is decreased brain cell volume, with the attendant risk for
intracerebral hemorrhage. Thus, the major symptoms are neurologic and
include confusion, seizures, focal neurologic deficits, and a progressively
decreasing level of consciousness that can progress to coma. In the absence
of an underlying neurologic problem or disturbance in the thirst mechanism,
the patient would be expected to complain of thirst unless the neurologic
injury has disturbed consciousness.
In patients with hypernatremia of sufficient duration to enable brain cells
to undergo osmotic adaptation, the risk for intracerebral hemorrhage from
cell shrinkage is decreased, but a hypertonic intracellular environment with
the accumulation of new intracellular solutes can perturb normal cellular
function.
DIAGNOSIS:
The diagnosis of hypernatremia is made by laboratory testing of the sodium
concentration, which always should be repeated to confirm its accuracy, corroborated
by measurement of plasma osmolality, which is expected to be
elevated in all cases. The underlying cause of the hypernatremia is usually
evident from the history and physical examination. The history should
include a review of recent and current medication use and questions regarding
exercise, heat exposure, sweating, vomiting, diarrhea, urine output, recent
fluid intake, and the presence of thirst. Physical examination should include
an assessment of ECF volume and a complete neurologic evaluation. Urine
volume should be monitored, urine osmolality should be measured in several
spot urine samples, and 24-hour urine osmolar excretion should be measured
if polyuria is present. In the less common situation of hypervolemic
hypernatremia, there is often an antecedent history of the administration of
sodium-containing solutions, and the findings on physical examination are
consistent with ECF volume expansion. In the absence of underlying intrinsic
renal disease or diuretic action, urine osmolality should be high because
of the hypertonic stimulus to AVP release, which overrides the attenuating
effect of hypervolemia. In such patients, the urine sodium concentration
should be elevated in response to hypervolemia.
In the more common condition of hypovolemic hypernatremia with extrarenal
fluid loss, urine output should be reduced to less than 500 mL/day, and
urine osmolality should be the maximum expected for age (urine osmolality
>1000 mOsm/kg in young adulthood and decreasing to >600 mOsm/kg by
the seventh decade of life and beyond). Polyuria with a submaximal urine
osmolality in the presence of hypernatremia suggests impaired urine-concentrating
ability, such as occurs with preexisting or underlying intrinsic renal
disease or exposure to diuretic agents. A spot urine osmolality measurement
less than 100 to 200 mOsm/kg or polyuria (>3 L/day), together with
24-hour urine solute excretion less than 600 mOsm/day in the face of hypernatremia,
suggests diabetes insipidus. In contrast, daily solute excretion
exceeding 800 to 1000 mOsm/day suggests an osmotic diuresis, which can
be confirmed by measuring glucose and urea in urine.
TREATMENT:
The main components of treatment are to treat the underlying disorder,
correct the abnormality in ECF volume, replace the water deficit, and provide
maintenance fluids to match continuing ongoing fluid losses if they persist.
The therapeutic approach to serious symptomatic hypovolemic hypernatremia
is challenging and often controversial. It is best to divide the therapeutic
approach into two separate phases: rapid correction of the depleted ECF
volume, followed by gradual replacement of the water deficit, including provision
for ongoing fluid losses. When ECF volume contraction is severe, as evidenced
by tissue hypoperfusion and shock, administered fluid should have a
sodium concentration as close as possible to that of the patient and should
distribute to the ECF or even the intravascular compartment. Isotonic saline is
generally the fluid of choice, and the volume and rate of administration should
be guided by clinical parameters related to reversal of hypovolemia. After the
patient’s tissue perfusion has been restored, further fluid replacement should
be aimed at correcting the estimated water deficit. This estimate begins with
a simple calculation of the percent deficit based on the measured sodium
concentration:
Total body water deficit premorbid = 0.6 × weight ×(1−[140/Na+ ])
Total body water is used because the sodium concentration reflects tonicity
in all body fluid compartments, including the ICF. Unlike the isotonic fluid
replacement for ECF volume, the water replacement should be administered
gradually over a period of hours to days, unless there is clear documentation
that the hypernatremia has itself evolved over minutes to hours. The necessity
for gradual replacement is dictated by the process of osmotic adaptation
described previously, and ideally, the rate of water replacement should match
the rate at which brain intracellular solutes can be adaptively extruded or
removed. More rapid rates of administration could result in brain cell swelling
with attendant dangerous neurologic consequences. It is recommended that
the estimated volume of the water deficit be replaced at a rate that will lead
to an approximately 0.5 to 1.0 mmol/L reduction in measured plasma sodium
concentration per hour. In addition to the estimated water deficit, the estimated
ongoing water loss during replacement should include at least 1 L per
24 hours of insensible fluid losses (greater volumes in patients who are febrile
or mechanically ventilated), supplemented with any ongoing water losses
(renal or gastrointestinal) resulting from continuation of the underlying
disease process. Because of the need to distribute replacement of the initial
water deficit, which can amount to several liters over a number of days during
which ongoing water losses continue, it is not unusual for patients to require
large volumes of water, sometimes reaching 5 to 10 L, over the duration of the
correction period. This water deficit, together with ongoing losses, can be
replaced by the dietary ingestion of tap water if the patient’s condition is suitable
or by an enteral feeding tube. If a gastrointestinal or other disease process
precludes these preferred routes, a hypotonic intravenous solution such as
D5W or half-normal saline can be used. When D5W is used, the glucose is either
stored as glycogen or fat or metabolized into carbon dioxide and water, thus
effectively providing the patient with solute-free water replacement. In the
case of half-normal saline, for any given liter administered, only half can be
considered as replacement of the water deficit, and the sodium content will
either replace any remaining sodium deficit that has not been fully corrected
in the first phase of treatment or be excreted if there is no impairment in
urinary sodium excretion. In elderly patients with known or possible underlying
cardiac, hepatic, or renal disease, caution should be exercised in the provision
of excessive volumes of salt-containing solutions. In any case, the sodium
concentration should be monitored at regular intervals of no less than every
4 hours to avoid too slow or too rapid correction, and ECF volume parameters
should be monitored to avoid hypervolemic complications.
Special considerations apply for hypertonic states in the setting of uncontrolled
diabetes with hyperglycemia (Chapters 236 and 237). The unusual cases
of patients with hypervolemic hypernatremia in the hospital setting also need
special attention and sometimes require continuous infusions of loop diuretics
together with the administration of hypotonic solutions or, in some cases,
extracorporeal means to remove both the sodium and water excess in a controlled
and safe manner under careful monitoring, often in the intensive care
unit.
The route of administration should change in accordance with the patient’s
response. Although an initial parenteral or nasogastric enteral route might be
appropriate when the patient’s neurologic status is compromised, subsequent
therapy can consist of simple dietary intake of water. Once a patient is awake
and alert and if thirst mechanisms are intact, the patient will generally correct
the hypertonic state by spontaneous oral fluid intake.
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