Hypernatremia &

Hyponatremia
(A Short Review) by DG Ghalan
 Hypernatremia
 Introduction

 It is anelectrolyte disturbance that is

defined by an elevated sodium level in
the blood. Hypernatremia is generally not
caused by an excess of sodium, but
rather by a relative deficit of free water in
the body.
 For this reason, hypernatremia is often
synonymous with the less precise
term,dehydration
 Water is lost from the body in a variety of ways,
including perspiration, insensible losses from
breathing, and in the feces and urine. If the
amount of water ingested consistently falls
below the amount of water lost, the serum
sodium level will begin to rise, leading to
hypernatremia. Rarely, hypernatremia can
result from massive salt ingestion, such as may
occur from drinking seawater.
 Ordinarily, even a small rise in the serum
sodium concentration above the normal range
results in a strong sensation of thirst, an
increase in free water intake, and correction of
the abnormality. Therefore, hypernatremia
most often occurs in people such as infants,
those with impaired mental status, or the
elderly, who may have an intact thirst
mechanism but are unable to ask for or obtain
water.
 Etiology
 (1.)Hypovolemic
 Inadequate intake of water, typically in elderly
or otherwise disabled patients who are unable
to take in water as their thirst dictates. This is
the most common cause of hypernatremia.
 Excessive losses of water from the urinary
tract, which may be caused by glycosuria, or
other osmotic diuretics.
 Water losses associated with extreme
sweating.
 Severe watery diarrhea
 (2.) Euvolemic:
 Excessive excretion of water from the
kidneys caused bydiabetes insipidus,
which involves either inadequate
production of the hormone, vasopressin,
from the pituitary gland or impaired
responsiveness of the kidneys to
vasopressin.
 (3.) Hypervolemic:
 Intake of a hypertonic fluid (a fluid with a higher
concentration of solutes than the remainder of the
body). This is relatively uncommon, though it can occur
after a vigorous resuscitation where a patient receives
a large volume of a concentratedsodium
bicarbonate solution. Ingesting seawater also causes
hypernatremia because seawater is hypertonic.
 Mineralcorticoid excess due to a disease state such
as Conn's syndrome or Cushing's Disease
 Symptoms:

 Clinical manifestations of hypernatremia

can be subtle, consisting oflethargy,
weakness, irritability, and edema. With
more severe elevations of the sodium
level, seizures and coma may occur.
 Severe symptoms are usually due to
acute elevation of the plasma sodium
concentration to above 158 mEq/L
(normal is typically about 135-145
mEq/L). Values above 180 mEq/L are
associated with a high mortality rate,
particularly in adults. However such high
levels of sodium rarely occur without
severe coexisting medical conditions.
 Treatment:

 The cornerstone of treatment is

administration of free water to correct the
relative water deficit. Water can be
replaced orally or intravenously.
However, overly rapid correction of
hypernatremia is potentially very
dangerous. The body (in particular
the brain) adapts to the higher sodium
concentration.
 Rapidly lowering the sodium concentration with
free water, once this adaptation has occurred,
causes water to flow into brain cells and
causes them to swell. This can lead to cerebral
edema, potentially resulting in seizures,
permanent brain damage, or death. Therefore,
significant hypernatremia should be treated
carefully by aphysician or other medical
professional with experience in treatment
ofelectrolyte imbalances.
Hyponatremia
Introduction:

 It is an electrolyte disturbance in which

the sodium concentration in the serumis
lower than normal. Sodium is the
dominant extracellular cation and cannot
freely cross the cell membrane. Its
homeostasis is vital to the normal
physiologic function of cells.
 Normal serum sodium levels are between
135-145 mEq/L. Hyponatremia is defined
as a serum level of less than 135 mEq/L
and is considered severe when the
serum level is below 125 mEq/L.
 Hyponatremia is most often a complication of
other medical illnesses in which either fluids
rich in sodium are lost (for example because of
diarrhea or vomiting) or excess water
accumulates in the body at a higher rate than
can be excreted (for example in congestive
heart failure, syndrome of inappropriate
antidiuretic hormone, SIADH, orpolydipsia).
 Regarding sodium loss as a cause of
hyponatremia, it is important to note that
such losses promote hyponatremia in
only an indirect manner. In particular,
hyponatremia occurring in association
with sodium loss does not reflect
inadequate sodium availability as a result
of the losses.
 Rather, the sodium loss leads to a state
of volume depletion, with volume
depletion serving as signal for the
release of ADH (anti-diuretic hormone).
As a result of ADH-stimulated water
retention, blood sodium becomes diluted
and hyponatremia results.
 Rather, the sodium loss leads to a state
of volume depletion, with volume
depletion serving as signal for the
release of ADH (anti-diuretic hormone).
As a result of ADH-stimulated water
retention, blood sodium becomes diluted
and hyponatremia results.
 Hyponatremia can also affect athletes
who consume too much fluid during
endurance events,people who fast on
juice or water for extended periods and
people whose dietary sodium intake is
chronically insufficient.
Frequency:

 Hyponatremia is the most common electrolyte

disorder. Its frequency is higher in females, the
elderly, and in patients that are hospitalized.
The incidence of hyponatremia depends
largely on the patient population. A hospital
incidence of 15-20% is common, while only 3-
5% of patients who are hospitalized have a
serum sodium level of less than 130 mEq/L.
 Hyponatremia has been reported in up to
30% of elderly patients in nursing homes
and is also present in approximately 30%
of depressed patients on selective
serotonin reuptake inhibitors.
Symptoms:
 Symptoms of hyponatremia include nausea
and vomiting, headache, confusion, lethargy,
fatigue, appetite loss, restlessness and
irritability, muscle weakness, spasms, or
cramps, seizures, and decreased
consciousness or coma. The presence and
severity of symptoms are associated with the
level of serum sodium, with the lowest levels of
serum sodium associated with the more
prominent and serious symptoms.
 However, emerging data suggests that
mild hyponatremia (serum sodium levels
at 131 mEq/L or above) is associated
with numerous complications and
undiagnosed symptoms.
 Many medical illnesses, such as
congestive heart failure, liver failure,
renal failure, or pneumonia may be
associated with hyponatremia. These
patients frequently present because of
primary disease symptomatology and are
diagnosed after presenting due to
manifestations of other medical issues.
 Neurological symptoms often show for
extremely low levels of sodium. When
sodium levels in blood become too low,
excess water enters cells and causes the
cells to swell. Swelling in the brain is
especially dangerous because the brain
is confined by the skull and is unable to
expand.
 Neurological symptoms most often are
due to very low serum sodium levels
(usually <115 mEq/L), resulting in
intracerebral osmotic fluid shifts and
brain edema. This neurological symptom
complex can lead to tentorial herniation
with subsequent brain stem compression
and respiratory arrest, resulting in death
in the most severe cases.
 The severity of neurological symptoms
correlates with the rapidity and severity of the
drop in serum sodium. A gradual drop, even to
very low levels, may be tolerated well if it
occurs over several days or weeks, because of
neuronal adaptation. The presence of
underlying neurological disease, like a seizure
disorder, or non-neurological metabolic
abnormalities, also affects the severity of
neurologic symptoms.
Examination

 Examination should include orthostatic

vital signs and an accurate assessment
of volume status. This determination (i.e.
hypervolemic, euvolemic, hypovolemic)
often guides treatment decisions. A full
assessment of medical comorbidity also
is essential, with particular attention paid
to cardiopulmonary and neurological
components of the examination.
Types of occurrence

 (I) Hypervolemic hyponatremia:

 excess water dilutes the sodium
concentration, causing low sodium levels.
Hypervolemic hyponatremia is commonly
the result of kidney failure, heart failure or
liver failure.
 (II) Euvolemic hyponatremia: normal
water levels are combined with low
sodium levels. This condition is
commonly due to chronic health
conditions, cancer or certain medications.
 (III)Hypovolemic hyponatremia:
 water and sodium levels are both low.
This may occur, for example, when
exercising in the heat without
replenishing fluid electrolytes or with
marked blood loss.
 In Chronic hyponatremia sodium levels drop
gradually over several days or weeks and
symptoms and complications are typically
moderate. Chronic hyponatremia is often called
asymptomatic hyponatremia in clinical settings
because it is thought to have no symptoms;
however, emerging data suggests that
“asymptomatic” hyponatremia is not actually
asymptomatic.
 In Acute hyponatremia sodium levels
drop rapidly, resulting in potentially
dangerous effects, such as rapid brain
swelling, which can result in coma and
death.
Causes:

 Many possible conditions and lifestyle factors

can lead to hyponatremia, including:
 Syndrome of inappropriate anti-diuretic
hormone (SIADH). In this condition, high levels
of the anti-diuretic hormone (ADH) are
produced, causing the body to retain water
instead of excreting it in urine.
 Cirrhosis. Liver disease can cause fluids to
accumulate in the body.
 Kidney problems. Kidney failure and other
kidney diseases can render the body unable to
efficiently remove excess fluids from the body.
 Congestive heart failure. This condition causes
the abdomen and lower extremities to retain
fluids.
 Water pills (diuretics), especially thiazide
diuretics. Diuretics work by making the body
excrete more sodium in urine
 Consuming excessive water during
exercise (exertional hyponatremia
or exercise-associated
hyponatremia (EAH)).Because sodium is
lost through sweat, drinking too much
water during endurance activities, such
as marathons and triathlons, can dilute
sodium content in blood.
 Hormonal changes due to adrenal gland
insufficiency (Addison’s disease). Adrenal
glands produce hormones that help maintain
the body’s balance of sodium, potassium and
water.
 Hormonal changes due to an under active
thyroid (hypothyroidism).
 Primary polydipsia. In this condition, thirst
increases significantly, causing a person to
drink excessive amounts of fluid.
 Certain medications. Some medications,
particularly selective serotonin reuptake
inhibitors and some pain medications, cause a
person to urinate or perspire more than normal.
 The recreational drug MDMA. This
amphetamine causes a ripple effect on the
body’s ADH and water levels that—especially
in combination with heavy drinking—increases
the risk of severe and even fatal cases of
hyponatremia.
 Chronic, severe vomiting or diarrhea. This
causes the body to lose fluids and electrolytes,
including sodium.
 Dehydration. In dehydration, the body loses
fluids and electrolytes.
 Diet. A low-sodium, high-water diet can disturb
the proper balance between sodium and fluids
in the blood. Excessive intake of diuretics,
including beer, can have the same effect.
Risk Factors:

 Age. Low blood sodium is more common in

older adults. Contributing factors include age-
related changes and a greater likelihood of
developing a chronic disease that impairs the
body’s sodium balance.
 Diet. A person may be at an increased risk of
hyponatremia if he is following a low-sodium
diet, especially in combination with drinking
diuretic beverages.
 Intensive physical activities. People who
drink too much water while taking part in
marathons, triathlons, Iron Man
competitions and other long-distance,
high-intensity activities are at an
increased risk of hyponatremia.
 Climate. New exposure to hot weather
can increase the amount of sodium a
person loses through sweating.
 Certain drugs. Medications that increase
risk of hyponatremia include thiazide
diuretics and selective serotonin reuptake
inhibitors and pain medications that
cause a patient to urinate or perspire
more than usual. In addition, the
recreational drug MDMA has been linked
to fatal cases of hyponatremia. .
Complication:

 Chronic hyponatremia can lead to such

complications as neurological impairments.
These neurological impairments most often
affect gait and attention and can lead to falls,
osteoporosis, and decreased reaction time.
 Complications for chronic hyponatremia are
most dangerous for geriatric patients. Falls are
the leading cause of deaths related to injury
among people 65 years or older.
 In a recent study the incidence of hyponatremia in
elderly patients with large-bone fractures was more
than double that of non-fracture patients. Recent work
by Verbalis etc suggests that hyponatremia induces
osteoporosis and found the adjusted odds ratio for
developing osteoporosis to be 2.87 times higher
among adults with mild hyponatremia compared to
those without.
 Acute hyponatremia can lead to much more serious
complications including brain disease, brain herniation,
cardiopulmonary arrest, cerebral edema, seizures,
coma, and death.
Treatment:

 The treatment of hyponatremia often

depends on the underlying cause. If a
person is truly asymptomatic or has only
subtle symptoms, little treatment other
than water restriction may be required. In
a setting of volume depletion,
intravenous administration of normal
saline may be effective.
 Pharmaceutically, vasopressin receptor
antagonists can be used in the treatment
of hyponatremia, especially in patients
with congestive heart failure or liver
cirrhosis. A vasopressin receptor
antagonist is an agent that interferes with
the action at the vasopressin receptors.
Vasopressin is also known as ADH, the
anti-diuretic hormone.
 A new class of medication, the “vaptan” drugs
has been specifically developed to inhibit the
action of vasopressin on its receptors (V1A,
V1B, and V2). These receptors have a variety
of functions, with the V1A and V2 receptors are
expressed peripherally and involved in the
modulation of blood pressure and kidney
function respectively, while the V1A and V1B
receptors are expressed in the central nervous
system. V1A is expressed in many regions of
the brain, and has been linked to a variety of
social behaviors in humans and animals.
 (Reference: Wikipedia)
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