hyponatremia and hypernatremia 2015
TRANSCRIPT
HYPONATREMIA AND HYPERNATREMIA
SAMIR EL ANSARY
Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY
•Why is sodium balance critical
to volume control?
Sodium and its corresponding anions
represent almost all of the osmotically
active solutes in the extracellular fluid
under normal conditions.
Therefore the serum
concentration of sodium reflects
the tonicity of body fluids.
Small changes in osmolality are
counteracted by thirst regulation,
antidiuretic hormone (ADH) secretion, and
renal concentrating or diluting
mechanisms.
Preservation of normal serum osmolality
(i.e., 285-295 mOsm/L) guarantees
cellular integrity by regulating net
movement of water across cellular
membranes.
ADH
Its mechanism of action
•ADH is also called arginine vasopressin or
simply vasopressin.
•ADH is a small peptide hormone
produced by the hypothalamus that binds
to the vasopressin 1 and 2 receptors
(V1 and V2).
•Vasopressin release is regulated by
osmoreceptors in the hypothalamus, which
are sensitive to changes in plasma osmolality
of as little as 1 % to 2%.
•Under hyperosmolar conditions,
osmoreceptor stimulation leads to stimulation
of thirst and vasopressin release.
These two mechanisms result in increased
water intake and retention, respectively.
•Vasopressin release is also regulated by
baroreceptors in the carotid sinus and aortic
arch; under conditions of hypovolemia, these
receptors stimulate vasopressin release to
increase water retention by the kidney.
•At very high concentrations,
vasopressin also causes vascular
smooth muscle constriction through the
V1 receptor, increasing vascular tone
and therefore the blood pressure.
Accordingly, vasopressin is often
administered parenterally as a
vasopressor agent in patients with
hypotension that is refractory to volume
resuscitation.
•Does hyponatremia simply mean
there is too little sodium in the
body?
No. The serum sodium
concentration is not a reflection of
the total body sodium content;
instead,it is more representative
of changes in the total body water.
With hyponatremia, defined as serum sodium
level less than 135 mEq/L, there is too much
total body water relative to the amount of total
body sodium, thereby lowering its
concentration.
Despite this key observation, the serum sodium
concentration is not a reflection of volume
status, and it is possible for hyponatremia to
develop in states of volume depletion,
euvolemia, and volume excess.
Assessing a patient's volume status is therefore
the key step in identifying the underlying cause
of hyponatremia .
it is possible for hyponatremia to
develop in states of volume depletion,
euvolemia, and volume excess.
Helpful physical findings include
tachycardia, dry mucous membranes,
orthostatic hypotension, increased skin
turgor (associated with hypovolemia) or
edema, an S3 gallop, jugular venous
distention, and ascites
(present in hypervolemic states).
•Are hyponatremia and
hypoosmolality synonymous?
No. Hyponatremia can occur
without a change in total body
sodium or total body water in two
settings.
The first is pseudohyponatremia, which is a
laboratory artifact in patients with severe
hyperlipidemia or hyperproteinemia.
This laboratory abnormality has been essentially
eliminated by the use of ion-specific electrodes
(rather than flame photometry) to determine the
serum
sodium concentration.
substances (such as glucose or
mannitol) cause hyponatremia but not
hypoosmolality, a condition known as
translocational hyponatremia.
In such states, water is drawn out of cells
into the extracellular space, diluting the
plasma solutes and equilibrating osmolar
differences.
In addition, use of large quantities
of irrigant solutions that do not
contain sodium
(but instead contain
Glycine, sorbitol, or mannitol)
During gynecologic or urologic
surgeries can also cause severe
hyponatremia.
Hyponatremia in a patient with
hypovolemia
Hypovolemic hyponatremia represents a
decrease in total body sodium in excess of
a decrease in total body water.
Simultaneous sodium and water loss can
be due to renal
(such as diuretic use) or extrarenal causes.
Hypovolemia results in a decrease in renal
perfusion, a decrement in the glomerular filtration
rate, and an increase in proximal tubule
reabsorption of
sodium and water; all three mechanisms
contribute to decreased water excretion.
Furthermore, hypovolemia supersedes the
expected inhibition of vasopressin release by
hypoosmolality and maintains the secretion of the
hormone.
The body protects volume at the
expense of osmolality.
HypovolemiaSupersedes the expected
inhibition of vasopressin release
by hypoosmolality
And maintains the secretion of
the hormone.
The body protects
volume
At the expense of
osmolality.
How does hypervolemic
hyponatremia differ from
hypovolemic
hyponatremia?
In hypervolemic hyponatremia, the kidneys are
at the center of the problem because of either
intrinsic renal disease or the renal response to
extrarenal pathophysiology.
Physical examination reveals edema and no
evidence of volume depletion.
Intrinsic renal disease with a compromised
glomerular filtration rate (acute or chronic)
prevents adequate excretion of sodium and
water.
Intake of sodium in excess of
what can be excreted leads to
hypervolemia (edema)
whereas excessive intake of
water leads to hyponatremia.
In contrast, in congestive heart
failure, hepatic cirrhosis, and
nephrotic syndrome, the intrinsically
normal kidney is stimulated to
retain sodium and water in response
to perceived decrements in
intravascular volume and renal
perfusion; as a result, hypervolemia
and hyponatremia develop.
In general, hypervolemic hyponatremia
due to an extrarenal cause is
characterized by a low urine sodium
concentration (<10 - 20 mEq/L)
This distinguishes it from hypervolemic
hyponatremia due to intrinsic renal
causes, where the urine sodium is > 20
mEq/L
{ In renal causes ,kidney can not
re-absorb Na } .
Syndrome of inappropriate
secretion of antidiuretic
hormone (SIADH)
SIADH is a common cause of
euvolemic hyponatremia
SIADH
And is associated with
malignancies, pulmonary disease,
central nervous system disorders,
pain, nausea, and many drugs.
SIADH
Common offending medications include
hypoglycemic agents, psychotropics
(including antipsychotics and
antidepressants), narcotics, and chemo-
therapeutic agents.
Other causes of euvolemic hyponatremia
include psychogenic polydipsia, a low-solute
diet (beer potomania or the tea and toast
diet), hypothyroidism, and adrenal
insufficiency.
Diagnostic tests
useful in the evaluation of
hyponatremia
The physical examination is critical to the
determination of volume status, as previously
described.
Serum electrolyte and serum and urine
osmolality measurements are useful.
High urine osmolality despite low serum
osmolality suggests either hypovolemic
hyponatremia or SIADH if the patient is in
a euvolemic state.
Very low urine osmolality suggests
excessive water intake, as in
psychogenic polydipsia or a low-solute
diet.
Measurements of thyroid stimulating
hormone and cortisol can be used to
assess endocrine causes of
hyponatremia.
In renal causes ,kidney can not
re-absorb Na
The urine sodium concentration can
help distinguish renal and
extrarenal causes of hypervolemic
hyponatremia.
Patients with diabetic ketoacidosis
frequently have hyponatremia
Diabetic ketoacidosis is an example of
hyperosmotic hyponatremia.
In general, serum sodium decreases by
approximately 2.4 mEq/L for every
increase of 100 mg/dL over normal
glucose levels.
In this setting, the serum sodium
level should not be interpreted
without an accompanying
serum glucose measurement, and
the appropriate correction should
be made if the glucose
exceeds 200 mg/dL.
Difference between acute
and chronic
hyponatremia
Acute hyponatremia
A distinct entity in terms of morbidity,
mortality, and treatment strategies.
Most commonly occurs in the hospital
(frequently in the postoperative
setting)
In psychogenic polydipsia, and in
elderly women taking thiazide diuretic
agents.
Chronic hyponatremia
Hyponatremia lasting longer than
48 hours.
The majority of patients who are seen
by physicians or emergency
departments with hyponatremia should
be assumed to have chronic
hyponatremia.
Signs and symptoms of
hyponatremia
Majority of patients have no
symptoms
symptoms
often develop in patients with a
serum sodium concentration
< I25 mEq/L or in whom the
sodium has decreased rapidly.
Gastrointestinal symptoms of nausea,
vomiting, and anorexia occur early
But neuropsychiatric symptoms such as
lethargy, confusion, agitation, psychosis,
seizure, and coma are more common.
Clinical symptoms roughly correlate
with the amount and rate of
decrease in serum sodium levels.
Drugsassociated with hyponatremia
Thiazide diureticsfrequently cause hyponatremia by promoting
sodium excretion in excess of water.
Of note, because loop diuretics directly impair
the creation and maintenance of the medullary
osmotic gradient, they are far less likely to cause
hyponatremia, as little stimulus for water
reabsorption occurs as urine passes through the
collecting duct.
Selective serotonin reuptake inhibitors
and several chemotherapeutic agentscause hyponatremia, and this is thought to occur
through the inappropriate release of ADH.
Nonsteroidal anti-inflammatory drugs block
the production of renal prostaglandins and allow
vasopressin to act unopposed in the kidney,
which
can lead to water retention.
Tricyclic antidepressants and a number
of anticonvulsants are also
associated with hyponatremia.
Last, use of { 3,4-methylene-dioxy-
meth-amphetamine, or Ectasy } ,
particularly in combination with
consumption of large volumes of water, is
associated with severe, life-threatening
hyponatremia.
Therapy for
Hyponatremia
Not all patients with hyponatremia should be
treated alike.
Duration (acute vs. chronic) and the presence or
absence of neurologic symptoms are the most
critical factors in determining the therapeutic
strategy.
The prescribed therapy must take into
consideration the patient's current
symptoms and the risk of provoking a
demyelinating syndrome with
overly rapid correction.
The first priority is circulatory
stabilization with normal saline
solution in patients with significant
volume depletion.
In patients with acute symptomatic
hyponatremia, the risks of delaying treatment,
which could lead to cerebral edema, subsequent
seizures, and respiratory arrest, clearly outweigh
any risk of treatment.
Hypertonic (3%) saline solution
with or without furosemide
(which promotes free water excretion)
should be given until symptoms
subside.
It is possible to calculate the expected
change in serum sodium
concentration on the basis of the
volume of and rate at which
hypertonic saline solution is infused,
and this should be done before its
administration.
In contrast, patient with
Asymptomatic chronic hyponatremia
in
high-risk categories
(e.g., alcoholism, malnutrition, and liver
disease) is at greatest risk for
complications of the correction of
hyponatremia, namely
Central pontine myelinolysis. Such patients are best treatedwith
Water restriction
Vasopressin V2 receptor
antagonists
( Aquaretics or vaptans )
that are available in the United States for
treatment of hypervolemic and euvolemic
hyponatremia
These agents promote free water
excretion
and are useful in selected patients.
Helpful guidelines
for treatment of
hyponatremia
In patients with
Chronic asymptomatic hyponatremia
Simple free water restriction(e.g., 1000 ml/day) allows a slow and
relatively safe correction of the serum
sodium concentration.
This strategy, however, requires patient
compliance, which may be particularly
challenging in the outpatient setting.
In selected patients who are behaviorally or
physiologically resistant to free water
restriction,
Administration of salt tablets, an ADH
antagonist (e.g., demeclocycline, 600-
1200 mg/day)
or a maneuver to increase urinary solute
excretion, such as the ingestion of a
high-solute diet, may be necessary.
A difficult therapeutic dilemma is posed by
patients with neurologic symptoms and
hyponatremia of unknown duration.
Such patients are at risk for development of a
Demyelinating disorder if treated too
aggressively
yet the presence of symptoms is reflective of
central
nervous system dysfunction.
A difficult therapeutic dilemma is posed by
patients with neurologic symptoms and
hyponatremia of unknown duration.
These patients should be given treatment with
hypertonic saline solution (and furosemide if
necessary), and their serum sodium level
should be monitored every 1 to 2 hours
initially.
The rate of increase should not
exceed 8 to 10 mEq/L in a 24-hour
period.Acute therapy can be slowed once symptoms
have improved or a safe serum sodium level
(typically 120-125 mEq/L) is stably attained
(note that if the serum sodium level is extremely
low, this may require too aggressive correction
for the first 24 hours).
Central pontine myelinolysis
Central pontine myelinolysis is a rare
neurologic disorder of unclear cause
characterized by
Symmetric midline demyelination of the
central pons.
Extrapontine lesions can occur in the basal
ganglia, internal capsule, lateral geniculate
body, and cortex.
Symptoms include motor
abnormalities that can progress to
flaccid quadriplegia, respiratory
paralysis, pseudobulbar palsy,
mental status changes, and coma.
Central pontine myelinolysis is often fatal
in 3 to 5 weeks; of the patients who
survive, many have significant residual
deficits.
Alterations in the white matter are best
visualized by magnetic resonance imaging.
Central pontine myelinolysis is one of the most
feared complications of therapy for
hyponatremia.
Risk factors include a change in serum sodium
level of > 12 mEq/L in 24 hours, correction of
serum sodium level to a normal or
hypernatremic range, symptomatic and
coexistent alcoholism, malnutrition, and liver
disease.
Can hypernatremia
also occur in
Hypovolemic, Euvolemic,
and hypervolemic states?
Hypernatremia
Defined as a serum sodium
concentration greater than 145
mEq/L, occurs when too little total
body water exists relative to the
amount of total body sodium, thereby
raising the sodium concentration.
•Given that even small rises in the serum
osmolality trigger the thirst mechanism,
•Hypernatremia is relatively uncommon
unless the thirst mechanism is impaired or
access to free water is restricted.
As a result, hypovolemic hypernatremia
tends to occur in the very young, the very
old, and the debilitated.
It is typically due to extracellular fluid
losses accompanied by inability to
take in adequate amounts of free
water.
Febrile illnesses, vomiting,
diarrhea, and renal losses are
common causes.
Euvolemic hypernatremia can also be due to
extracellular loss of fluid without adequate
access to water or from impaired water
hemostasis.
Diabetes insipidus, either central (i.e.,
inadequate ADH secretion) or nephrogenic (i.e.,
renal insensitivity to ADH), results in the inability
to reabsorb filtered water, which causes
systemic hyperosmolality but
hypoosmolar (dilute) urine.
Hypervolemic hypernatremia
Although uncommon, is iatrogenic. Sodium
bicarbonate injection during cardiac arrest,
administration of hypertonic saline
solution, saline abortions, and
inappropriately prepared infant formulas
are several examples of induced
hypernatremia.
Causes of diabetes insipidus
Central diabetes insipidus
Can result from trauma, tumors, strokes,
granulomatous disease, and central
nervous system infections, and it
commonly occurs after neurosurgical
procedures.
Causes of diabetes insipidus
Nephrogenic diabetes insipidus
Can be congenital or it can occur in
acute or chronic renal failure,
hypercalcemia, hypokalemia, and sickle
cell disease, or after treatment with
certain drugs (e.g., lithium,
demeclocycline).
Signs and symptoms of
hypernatremia
In awake and alert patients, thirst is
a prominent symptom.
Anorexia, nausea, vomiting, altered
mental status, agitation, irritability,
lethargy, stupor, coma, and
neuromuscular hyperactivity are also
common symptoms.
The best therapy for hypernatremia
The first priority is circulatory stabilization
with normal saline solution in patients with
significant volume depletion.
Once normotensive, patients can be
rehydrated with oral water, intravenous 5%
dextrose in water (D5W), or even one-half
normal saline solution.
Overly rapid correction of long-standing
hypernatremia can result in cerebral
edema. Water deficit can be calculated
Some investigators have suggested that in
patients with long-standing hypernatremia,
the water deficit should be corrected by
no more than
10 mEq/L/day or 0.5 mEq/L/hr.
If the hypernatremia has occurred over a short
period (hours), it can be corrected more rapidly,
with the goal of correcting half of the water deficit
in the first 24 hours.
In addition to correcting the already established
free water deficit, daily
ongoing losses of free water in the urine and
stool and from the respiratory tract and skin
(particularly in patients with fever) should be
replaced.
In patients with central diabetes
insipidus, a synthetic analog of
ADH (i.e., 1-deamino-8-D-arginine
vasopressin) can be administered,
preferably by the intranasal route.
Helpful formulas for
assessing sodium
abnormalities
Serum osmolality
= 2 [Na+] + Glucose/l8 + Blood urea nitrogen /
2.8 + Ethyl alcohol / 4.6
Total body water (TBW)
= Body weight x 0.6 (for men)
TBW = Body weight x 0.5 (for women and the
elderly)
TBW excess in hyponatremia= TBW (1 - [Serum Na+] / 140)
Expected change in serum sodium level after
1 L 3% saline solution= (513 mEq/L – Serum [Na+]) / (TBW + 1)
TBW deficit in hypernatremia = TBW (Serum
[Na+] / 140 - 1)
Expected change in serum sodium level after
1 L D5W
= (Serum [Na+]) / (TBW + 1)
Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY
