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Hyponatremia

Night Time Education


Claire Stewart
January 21, 2013

What is it?
Serum sodium <135
How does the body prevent
hyponatremia?
The kidneys ability to generate dilute
urine and excrete free water
Usually hyponatremia occurs when there
is an excess of free water with impaired
ability to excrete free water/make dilute
urine

AVP (aka ADH)


Adenosine vasopressinproduced in
the hypothalamus and released from
the posterior pituitary
Inhibits water diuresis by Increasing
permeability to water in the kidney

Normal physiology
Extra fluid causes a drop in serum
osmolality leading to suppression of
ADH and secretion of more dilute
urine
Example: increased water intake
lowers the plasma osmolality,
decreases ADH secretion and
reduces collecting tube permeability
to waterexcretion of excess water
in dilute urine

Evaluation
Serum osms Hyponatremia associated with
hyperosmolality can be secondary to
hyperglycemia, hyperlipidema or
hyperproteinemia
(2 x serum Na)+(serum glucose/18)+
(BUN/2.8)

Urine osmolality
Urine sodium

Evaluation
Volume status
Decreased weight (hypovolemia)
Decreased circulating volume stimulates ADH secretion
leading to worsening hyponatremia
GI losses
Skin losses (CF)
Third spacing

Decreased urine sodium (usually <25), decreased


urine volume and more concentrated urine (increase
osmolality)
Special case: hypovolemic hyponatremia with metabolic
alkalosis 2/2 vomitingurine sodium may be greater than
25 but urine chloride concentration is low

Evaluation
Volume status
Decreased weight
Renal losses-nephropathy or diuretics
Findingsincreased urine sodium (>25),
increased urine volume with dilue urine and
decreased urine osmolality

Evaluation
Increased or normal weight
Nephrotic syndrome
SIADH
Water intoxication
Heart failure
Hypotonic fluid administration

Low serum osmolality; decreased urine


volume with increased urine osmolality
(>100)urine sodium >25

Treatment
Hypovolemic hyponatremiaadminister isotonic fluids
Treat the underlying cause no matter
fluid status
Normovolemic hyponatremia-treat
underlying cause
Hypertonic saline (3%) only if
neurologic symptoms

C:\Users\cstewart\Desktop\PubMed Ce
ntral, TABLE 1
Paediatr
Child Health. 2008 July; 13(6) 502
506..htm

SIADH
Hospitalized children have numerous
nonosmotic stimuli for ADH secretion
Low serum osmolality; decreased
urine volume with increased urine
osmolality (>100)urine sodium
>25
Also see low to normal creatinine and
potassium

SIADH-Causes
CNS disease-head injury, meningitis,
encephalitis, subarachnoid hemorrhage,
neurosurgery
Pulmonary disease-pneumonia, bronchiolitis
Stress
Post-op-anesthetic agents, pain, nausea,
opiates
Medications-carbamazepine,
oxcarbemazepine, SSRIs, chemotherapeutics
(Cytoxan, vincristine), immune modulators

SIADH
Usually unresponsive to increased
sodium administration when not used
in conjunction with fluid restriction

Cerebral Salt Wasting


Etiology unknown
BNP released from hormone producing
neurons in the brain in response to
increased ICPBNP acts on renal tubular
sodium reabsorption
? Protective measure to limit rise in ICP

Renal salt wastingvolume


depletionrelease of
ADHhyponatremia

Cerebral Salt Wasting


Usually happens approx 10 days
after insult
Labs findings
Hyponatremia (<135)
Low plasma osmolality
Elevated urine osmolality
Urine sodium >40
PLUS CLINICAL EVIDENCE OF
HYPOVOLEMIA (urine output, skin turgor,
CVP)

Treatment
Volume repletion with isotonic
saline/sodium administration
suppresses release of ADH leading to
excretion of excess water and
correction of hyponatremia
Usually resolves in 3-4 weeks

Hyponatremic
Encephalopathy
Hyponatremiainflux of water into
the intracellular spacecellular
swellingcerebral edema and
encephalopathy
Headache, N/V, weakness-->
seizures, altered mental status,
herniation
Children at higher risk than adults
and at higher serum sodiums

Hypernatremic
encephalopathy
2mL/kg of 2% NaClmax 100 mL
over 10 minutes

Osmotic demyelination
syndrome
Higher risk when sodium concentration increased
by more than 10-12 within 24 hours or more than
18 in 48 hours
An increase in 4-6 meq/L in 24 hours is goal (aim
for less than 9); should be sufficient to reverse the
most severe manifestations of acute
hyponatremia
Usually occurs with other co-morbidities, in
chronic hyponatremia and more commonly in
adults
Usually occurs 2-7 days after correction of sodium

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