Today's case involved an
elderly woman with multiple comorbidities including asthma, coronary artery
disease, and hypothyroidism. She
was brought in for ‘delirium’ and found to have a serum sodium of
113mmol/L.
Today’s case had
multiple learning points:
-Delirium is something
that we see frequently in medicine. Delirium is an acute change in mental status characterized by a fluctuating course, disordered thought, and agitation
or depressed level of consciousness. It has a very wide differential diagnosis,
and can be caused by quite a number of things.
The typical treatment of delirium is fixing
the underlying cause which can vary quite substantially depending on what
it is. Around 20% of the time, no
definitive cause is found for the delirium in elderly patients. Resolution of delirium does not always
correlate with resolution of the underlying illness, and may lead to further
disability and cognitive changes.
Finally, delirium is independently associated with higher risk of poor
outcomes from hospitalization, suggesting that it should be treated as a medical emergency on that basis.
-The mnemonic that
many people like is DIMS
Drugs – anticholinergics, benzodiazepines, ‘narcotics’, alcohol, and
withdrawal from drugs
Infections - CNS infections (meningitis,
encephalitis) and systemic infections
Metabolic – electrolyte disturbances, endocrinopathies, CO2 retention, etc.
Structural – Space occupying lesions, stroke, seizure, intracerebral bleeds
-Hyponatremia is a
common problem in hospitalized patients.
Think of hyponatremia as a water
disorder rather than a sodium
disorder. Essentially there is too much
free water for the amount of sodium in the body.
-Why do we care so
much about hyponatremia? There are a couple of reasons. Acutely, hyponatremia can produce alterations
in mental status and seizures a result of cerebral edema (too much water
outside brain cells, osmotic shift of water into brain cells, cerebral edema,
raised intracranial pressure, seizure).
The other component that we care about is overcorrection of hyponatremia which can lead to osmotic demyelination syndrome
(previously central pontine myelinolysis). For those who have never seen this
complication, it is a devastating injury to the brainstem that can result in
“locked-in” syndrome (only able to move eyes).
Risk factors include low muscle mass (cirrhotic, malnourished),
hypokalemia, and female sex. The classic
teaching recommended not increasing the sodium by more than 10mmol/L in a 24
hour period, but nephrologists are now stratifying patients by their risk for
ODS, and recommending more conservative correction for those at higher risk.
-There are a lot of
‘approach to hyponatremia’ documents out there but I will try to give you a
simplified one that I use. Firstly,
there are only THREE mechanisms that can produce hyponatremia:
(1) – free water is
unable to be excreted by the kidney leading to an elevated water:sodium ratio
in the body (this is the case in extreme renal failure).
(2) – Antidiuretic
hormone is turned on, and is the only
mechanism that separates salt from water retention. With this on, water is
preferentially reabsorbed by kidneys leading to an increased water:sodium ratio
in the body.
(3) – there is
insufficient solute to excrete the
free water. Our kidneys can only dilute
urine down to around 50 mOsm/L meaning that guzzling free water and eating
things without any solute (sodium,
proteins, etc.) will invariably lead to, you guessed it, an increased
water:sodium ratio in the body.
(1) – is the
hyponatremia real? (check the serum osmolality). Things that can cause
hyperosmolar or euosmolar hyponatremia are elevated paraproteins, lipids,
glucose, etc.
(2) – Now that it’s
real, is it symptomatic? (i.e. is the patient seizing)
If it’s symptomatic,
the treatment should be to rapidly correct the sodium by 1-2mmol/L until the
patient stops seizing. This is done in
ICU’s with 200cc of 3% NaCl solution rapidly infused.
(3) – Now that it’s
real, and asymptomatic, is it acute or chronic?
Most of the time you won’t know whether it’s acute or chronic because
people don’t get their labs checked at home.
That said, acute hyponatremia can be corrected acutely without risk of
ODS. Chronic hyponatremia (48-72h) must
be corrected slowly to avoid ODS.
(4) – Now that it’s
real, asymptomatic, and chronic, what is the patient’s volume status? What volume status is the kidney seeing? Ordering the urine lytes answers the second
question (if the kidney is seeing low volume, the urine sodium will be under
20). Diuretics will interfere with this. The rest of your physical exam answers the
first question. Many people will order
urine osmolality as well. This tells you
whether ADH is acting or not (it is high if ADH is acting). An example of hyponatremia when ADH is not acting would be psychogenic
polydipsia, or insufficient solute intake.
From here, it’s
helpful to break things down into causes by volume. Hypovolemia causes ADH to be released to
maintain plasma volume. This is not because extracellular water stays
intravascular, but because ADH acts as a potent vasoconstrictor to maintain
systemic vascular resistance. So
patients with diarrhea, vomiting, sepsis, etc. may have appropriate ADH on board.
Hypervolemic patients
like CHF, cirrhotic, or nephrotic syndrome patients are hypovolemic from a renal perspective, meaning that their kidneys
behave like the first group. Treatment
of their underlying problem may resolve the hyponatremia.
The euvolemic group
has a lot of causes: hypothyroidism, adrenal insufficiency, medications
(diuretics, antiepileptics, SSRI’s), “tea and toasters”, psychogenic
polydipsia, and the ever-famous SIADH (syndrome
of inappropriate antidiuretic hormone).
SIADH occurs for a
number of reasons: lung pathology, tumours, CNS disease, pain, nausea, etc.
So based on the above,
you can see that the treatment varies widely.
If you give someone with SIADH normal saline, their sodium may go down because that potent ADH will
reabsorb all the water, and allow excretion of all the sodium. On the contrary,
someone with hypovolemic hyponatremia will correct their sodium rapidly because the saline restores
intravascular volume, leading to a shutoff of their ADH release, and a water diuresis. That’s why we sometimes give salt cubes, or
urea, to patients with low solute intake – it drags out some of the excess
water and increases the capacity for free water excretion.
Further Reading:
Ellison, D. H., &
Berl, T. (2007). The syndrome of inappropriate antidiuresis. New England
Journal of Medicine, 356(20), 2064-2072.
Spasovski, G.,
Vanholder, R., Allolio, B., Annane, D., Ball, S., Bichet, D., ... & Nagler,
E. (2014). Clinical practice guideline on diagnosis and treatment of
hyponatraemia. European journal of endocrinology, 170(3), G1-G47.
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