Hyponatremia - Webstercare

JANUARY 2011
H
HYPONATRAEMIA
yponatraemia or low serum sodium is a common
electrolyte disorder in the older person with
significant morbidity and mortality.
Hyponatraemia may be present in up to 20% of residents
in aged care facilities. It is also present in up to 30% of
patients with depression on selective serotonin reuptake
inhibitors (SSRIs).
Hyponatraemia is generally defined as a plasma sodium
level of less than 135 mmol/L. The normal reference range
for serum sodium is between 135 and 145mmol/L.
Other laboratory tests that may be considered are serum
osmolality and urine osmolality, urine sodium concentration,
other electrolytes (potassium, chloride, bicarbonate), urea,
glucose, uric acid, total proteins and triglycerides. Serum
levels of thyroid-stimulating hormone (TSH) are needed to
identify hypothyroidism.
Age-related changes
Hyponatraemia is more common in older people because
they have an increased incidence of comorbid conditions
(heart failure, renal failure) that can be complicated by it.
As the body ages there is a decrease in total body water
that makes the older person susceptible to electrolyte
disturbances such as hyponatraemia.
In addition, the thirst mechanism diminishes with age and
increases the risk of dehydration. There is also an agerelated decrease in the ability to concentrate urine, which
also increases the risk of dehydration. The ability to excrete
a water load is delayed in the elderly.
Age-related changes to the kidneys occur, with decreased
kidney mass, decreased renal blood flow and glomerular
filtration rate, as well as impaired responsiveness to sodium
balance in the body.
Causes
Most of the water in the body is in the cells. If water moves
from the cells to the plasma, it dilutes the plasma, resulting
in hyponatraemia.
Antidiuretic hormone (ADH) prevents the clearance
of water from the body. This hormone is appropriately
released in older people who are hypovolaemic as a way
to encourage the body to conserve water. In contrast, ADH
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may be inappropriately released in response to cancer, certain
medications, or diseases such as hypothyroidism.
Hyponatraemia usually occurs when elimination of total
body water decreases and the kidneys retain too much water
or if there is increased oral intake of water. This may be due to
medications and the syndrome of inappropriate antidiuretic
hormone (SIADH) secretion.
Types of hyponatraemia
Hyponatraemia reflects the fluid status of the person and can
be classified as:
■■
Hypervolaemic (or dilutional) - excess water dilutes
the sodium concentration, causing low sodium levels
■■
Hypovolaemic (or depletional) - water and sodium
levels are both low
■■
Euvolaemic - normal water levels are combined
with low sodium levels
Hypervolaemic hyponatraemia can be caused by retention
of excessive water and occurs in heart failure, liver cirrhosis
and kidney disease (renal failure or nephrotic syndrome). The
person shows oedema or fluid overload due to an increase in
total body water.
Hypovolaemic hyponatraemia may be due to gastrointestinal
loss (diarrhoea, vomiting), excessive loss of sodium through
the skin (burns, excessive sweating), sodium loss by kidneys
(diuretics) or poor water intake.
To distinguish between hypovolaemic and euvolaemic
hyponatraemia plasma osmolality and urinary sodium
concentration need to be measured also.
Increased plasma osmolality may be caused by severe
hyperglycaemia that may occur in a person with diabetes and
diabetic ketoacidosis.
Low plasma osmolality with a high urine sodium level may
be due to hypothyroidism, SIADH or medications. A urine
sodium level greater than 40mmol/L is suggestive of SIADH
or hypothyroidism.
Low urinary sodium concentration is caused by severe
burns, gastrointestinal losses from vomiting and diarrhoea
and acute water overload.
Medication causes
Onset of drug-induced hyponatraemia usually occurs within
Hyponatraemia, continued
the first month of treatment.
Medications that cause hyponatraemia include:
■■
Thiazide diuretics (eg hydrochlorothiazide)
■■
Thiazide-like diuretics (eg indapamide)
■■
Carbamazepine (Tegretol)
■■
Chlorpromazine (Largactil)
■■
Vasopressin (Pitressin)
■■
Indapamide (Natrilix, Dapa-Tabs)
■■
SSRI and SNRI antidepressants
■■
Theophylline (Nuelin SR)
■■
Amiodarone (Aratac, Cordarone X, Cardinorm)
■■
Ecstasy
Frusemide is not likely to cause hyponatraemia.
NSAIDs, corticosteroids (eg prednisone) and fludrocortisone
(Florinef) can cause increase salt and fluid retention.
Common medication causes of SIADH include
amiodarone, carbamazepine, chlorpromazine, SSRI and
SNRI antidepressants and theophylline. Medications most
commonly reported are hydrochlorothiazide, indapamide,
paroxetine, venlafaxine and sertraline.
Non-drug causes include cerebral disorders (tumor,
meningitis) and chest disorders (pneumonia, empyema).
Symptoms
Most people with hyponatraemia do not show any signs
or symptoms. Symptoms do not generally appear until the
plasma sodium level drops below 120mmol/L.
Early signs include headache, lethargy, malaise and nausea.
Confusion, agitation, irritability and disorientation may also
occur.
In cases of severe hyponatraemia (less than 115 mmol/L),
neurologic and gastrointestinal symptoms occur. It can
cause significant and permanent neurological injury and
death.
If hyponatraemia develops rapidly, muscular twitches,
irritability and convulsions can occur. The risk of seizures
and coma increases as the sodium level decreases.
Levels of serum sodium only slightly below normal are
associated with increased mortality and increased length of
stay in hospital.
Falls and fractures
Older people even with mildly decreased levels of sodium
in the blood experience increased rates of falls and fractures.
They are twice as likely to experience a major fracture as
those who do not have low sodium blood levels.
The risk of vertebral fracture and vertebral compression
fractures is about 60% higher in adults with hyponatraemia.
Hip fractures are also considerably increased, with a 39%
difference.
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However hyponatraemia does not appear to affect bone
mineral density (BMD) nor the risk of osteoporosis, the
most common cause of fractures in older people.
Management
Identifying the cause of hyponatraemia is the first step in
the treatment plan. Patients with hyponatraemia from any
cause require close attention to their electrolyte and fluid
status.
Acute severe hyponatraemia (less than 125mmol/L) is
usually associated with seizures and should be treated
urgently with hypertonic saline, with or without loop
diuretics (frusemide). Diuretics may be necessary when
significant oedema is present.
In persons with chronic hyponatraemia, rapid correction
should be avoided. In most cases, removing the underlying
cause or medication is sufficient.
Fluid restriction (less than 1 to 1.5 litre per day) is the
main treatment and the preferred mode of treatment with
SIADH. It is generally effective and inexpensive, although
compliance can be poor unless supervised.
Other less common treatments include lithium and
demeclocycline. A new class of medications called vaptans
or vasopressin receptors antagonists increase the elimination
of electrolyte-free water, but are currently not available in
Australia.
The addition of salt tablets is not appropriate.
Summary
Hyponatraemia is a common electrolyte disturbance in
older people. In all residents with hyponatraemia the cause
should be identified and treated. Treatment of even mild
hyponatraemia should be considered. Hyponatraemia can
result in changes in cognition and seizures. Even mild levels
of chronic hyponatraemia may contribute to an increased
rate of falls.
References
American Family Physician 2004;69:2387-94.
Australian Adverse Drug Reactions Bulletin 2008;27(5):19-20.