Download HYPONATREMIA

HYPONATREMIA
Dr. M. A. SOFI MD; FRCP
(London); FRCPEdin; FRCSEdin
HYPONATREMIA
 Hyponatremia is commonly defined as a serum sodium
concentration below 135 meq/L but can vary to a small
degree in different clinical laboratories.

The dilutional fall in serum sodium is in most patients
associated with a proportional reduction in the serum
osmolality (i.e., to a level below 275 mosmol/kg), but there
are some exceptions

Hyponatremia represents a relative excess of water in
relation to sodium. It can be induced by a marked increase
in water intake (primary polydipsia) and/or by impaired
water excretion resulting from advanced renal failure or
from persistent release of antidiuretic hormone (ADH).
Disorders in which ADH levels are
elevated or appropriately suppressed
Hyponatremia with elevated or normal
plasma osmolality
Effective circulating volume depletion
High plasma osmolality (effective osmols)
True volume depletion
Hyperglycemia
Heart failure
Cirrhosis
Mannitol
High plasma osmolality (ineffective osmols)
Renal failure
Thiazide diuretics
Alcohol intoxication
Inappropriate ADH secretion
Normal plasma osmolality
Hormonal changes
Pseudohyponatremia (laboratory artifact)
Adrenal insufficiency
High triglycerides
Hypothyroidism
Cholestatic and obstructive jaundice
(lipoprotein X)
Pregnancy
Multiple myeloma
ADH levels appropriately suppressed
Absorption of irrigant solutions
Advanced renal failure
Glycine
Primary polydipsia
Beer drinker's potomania
Mannitol
Sorbitol
Acute or hyperacute hyponatremia:
developed within the previous 24 hours, it is called "acute."
developed over just a few hours due to a marked increase in water
intake (self-induced water intoxication, as may be seen in
marathon runners, psychotic patients, and users of ecstasy), it is
called "hyperacute."
Chronic hyponatremia:
present for more than 48 hours, or if the duration is unknown
(such as in patients who develop hyponatremia at home), it is
called "chronic."
Sub-acute :
developed within the previous 24 to 48 hours, it is called
"subacute."
Mild to moderate hyponatremia:
defined as a serum sodium concentration between 130 and 135
meq/L; moderate hyponatremia is often defined as a serum sodium
concentration between 121 and 129 meq/L.
Severe hyponatremia:
defined as a serum sodium of 120 meq/L or less.
EVALUATION — The diagnostic approach consists of a directed
history and physical examination, appropriate laboratory tests.






A history of fluid loss (e.g., vomiting, diarrhea, diuretic
therapy) and, on examination, signs of volume depletion,
such as decreased skin turgor, a low jugular venous pressure,
or orthostatic or persistent hypotension.
A history of low protein intake and/or high fluid intake.
A history consistent with one of the causes of SIADH.
Use of medications associated with hyponatremia.
Signs of peripheral edema and/or ascites, which can be due to
heart failure, cirrhosis, or renal failure.
Symptoms and signs suggestive of adrenal insufficiency or
hypothyroidism.
Symptoms : Hyponatremia


Absent symptoms –
Patients are frequently
asymptomatic, if the
hyponatremia is chronic
and of mild or moderate
severity (i.e., serum
sodium >120 meq/L).
However, such patients
may have subclinical
impairments in mentation
and gait.
Mild to moderate
symptoms –Relatively
nonspecific and include
headache, nausea,
vomiting, fatigue, gait


disturbances, and confusion
in patients with chronic
hyponatremia (i.e., >48 hours
duration).
However, in patients with
more acute hyponatremia,
such symptoms should be
considered ominous and may
evolve without warning to
seizures, respiratory arrest,
and herniation.
Severe symptoms – Severe
symptoms of hyponatremia
include seizures,
obtundation, coma, and
respiratory arrest.
Laboratory tests :
Three laboratory tests provide
important initial
information in the
differential diagnosis of
hyponatremia :
 Serum osmolality
 Urine osmolality
 Urine sodium, potassium,
and chloride
concentrations



Serum osmolality (Sosm),
(NR 275 to 290 mosmol/kg)
is reduced in most
hyponatremic patients.
In some patients Sosm is
high or normal.
The three most common
causes of hyponatremia
with a high or normal Sosm
 Marked hyperglycemia
 Severe azotemia
 Alcohol intoxication
Hyponatremia causes:
Hyperglycemia – In patients with marked hyperglycemia,
which is almost always a manifestation of uncontrolled diabetes,
the increase in serum glucose raises the Sosm, which pulls water
out of the cells and lowers the serum sodium concentration
Azotemia – In patients with advanced renal failure, the
hyponatremia is due to an inability to excrete water resulting
from the impairment in renal function. Although this will tend
to lower the Sosm, this effect is counterbalanced to a variable
degree by the associated elevation in blood urea nitrogen
(BUN), resulting in an Sosm that may be normal or elevated.
Alcohol intoxication – True hyponatremia is common in
patients with alcoholism. The reduction in the Sosm associated
with hyponatremia can be offset in some patients by high
circulating levels of ethanol.
Less common causes of hyponatremia with a high or normal
Sosm include:
Administration of either hypertonic mannitol or maltose or
sucrose in conjunction with intravenous immune globulin will
cause hyponatremia in patients with renal failure.
Irrigant absorption – The absorption of nonconductive
glycine, sorbitol, or mannitol irrigation solutions during TURP
(called the transurethral resection syndrome) or during
hysteroscopy or laparoscopic surgery can lower the serum
sodium by increasing the extracellular fluid volume with these
sodium free solutions.
Pseudohyponatremia – Hyperlipidemia or hyperproteinemia
lower the serum sodium concentration (and therefore the
calculated Sosm) without changing the measured Sosm. This
laboratory artifact is called pseudohyponatremia
Treatment Hyponatremia
Patients with acute or hyper-acute hyponatremia, most patients
with severe hyponatremia, and many symptomatic patients with
moderate hyponatremia should be treated in the hospital
Emergency therapy
 Patients with severe
symptoms such as seizures
or obtundation.
 Patients symptomatic with
acute hyponatremia. even if
such symptoms are mild.


Patients with hyperacute
hyponatremia due to selfinduced water intoxication,
even if there are no
symptoms at the time of
initial evaluation.
Symptomatic patients who
have either acute
postoperative hyponatremia
or hyponatremia associated
with intracranial pathology.
Treatment Hyponatremia
Patients with acute or hyper-acute hyponatremia, most patients
with severe hyponatremia, and many symptomatic patients with
moderate hyponatremia should be treated in the hospital
Non-emergency therapy
 Asymptomatic patients with
acute or sub-acute
hyponatremia: Initial
treatment with hypertonic
saline rather than other
therapies.


Patients with severe
hyponatremia (i.e., serum
sodium ≤120 meq/L) who
have either absent or mild to
moderate symptoms. initial
treatment with hypertonic
saline
Patients with moderate
hyponatremia who have mild
to moderate symptoms.
Initial therapy depends in
large part upon the
underlying etiology.
Treatment



In all hyponatremic patients
the serum sodium initially
be increased by 4 to 6
meq/L during the first 24
hours and by less than 9
meq/L over any given 24hour period.
In patients who require
non-emergency therapy,
this goal can be achieved
slowly.
Patients receiving
emergency therapy their
serum sodium measured
every two hours to ensure
increase at the desired rate.


Other patients who are
treated for chronic
hyponatremia in the
hospital should have their
serum sodium measured
often enough to ensure an
appropriate rate of
correction and to allow the
clinician to react quickly to
impending overly rapid
correction (e.g., every four
hours).
The urine output should
also be monitored
Figure 3
Severe symptomatic hyponatremia



An intravenous bolus of
100 mL of 3% saline is
given and repeated if
symptoms persist after 10
minutes.
Once symptoms improve,
the rate of sodium
correction in 24 hours with
this regimen should not
exceed 6 to 8 mEq/L in 24
hours or 12 to 14 mEq/L in
48 hours.
Check serum sodium every
two hours and monitor
urine output closely


If the patient is making
large volumes of urine,
serum sodium may be rising
too quickly.
This can be accomplished by
giving desmopressin to slow
urinary free water loss while
simultaneously giving
hypotonic fluids.
Asymptomatic or mildly symptomatic
hyponatremia:
Hypovolemic
hyponatremia:
Treatment is aimed at
correcting volume
status
 ADH secretion will
always choose to
preserve volume over
osmolarity.
 In most cases, normal
saline will restore
intravascular volume.

Rapid correction of
serum Na, so hypotonic
solutions (½ NS) should
be used.
 Once volume is replete,
ADH release will cease.
 Vaptans should not be
used in hypovolemic
hyponatremia, or in
conjunction with other
treatments for
hyponatremia.

Asymptomatic or mildly symptomatic hyponatremia
• Euvolemic
Hyponatremia:
Typically caused by
SIADH- high Uosm
(>100 mosm/L) and a
high UNa (>30 mEq/L).
• Free water restriction,
and fluid at least 500
mL below a patient’s
urine output.
• If this is ineffective, salt
tabs can be given to
increase the solute load.
• Nine grams of salt tabs
in 3 divided doses
(equivalent to 1 L of
NS).
• Patients with highly
concentrated urine
(Uosm >500 mosm/L)
will not respond to the
salt load.
• In such patients, a loop
diuretic can be used to
help excrete free water.
Asymptomatic or mildly symptomatic
hyponatremia






Hypervolemic
Hyponatremia: caused by
CHF, cirrhosis, or NS.
ADH is in all cases.
In CHF and cirrhosis, the
degree of hyponatremia is a
marker of disease.
Fluid restriction is the
cornerstone of therapy
If the patient’s volume status
is not optimized, then loop
diuretics may improve
hyponatremia through
excretion of diluted urine.


In addition, ACEI can
improve hyponatremia in
CHF by reducing ADH
levels and improving cardiac
output via after-load
reduction.
Recent interest in the use of
vasopressin V2 receptor
antagonists or “vaptans.”
The latest AHA guidelines
for CHF recommend (class
IIb) vaptans in patients with
“hyponatremia that may be
causing cognitive symptoms
when standard measures
have failed.