Transcript Hyponatremia Debra Bynum,MD Division of Geriatric Medicine Clinical Case   An 82 y/o woman is admitted from a nursing home with confusion.

Hyponatremia
Debra Bynum,MD
Division of Geriatric Medicine
Clinical Case
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An 82 y/o woman is admitted from a nursing home with
confusion. She has had a poor appetite over the past
year with significant weight loss. Two weeks ago HCTZ
was added. Over the past few days, the nurses note
some n/v, no diarrhea, fever or other complaints.
On exam, she has some dry oral mucosa but she is not
orthostatic. There is no evidence of CHF, ascites or
edema. She is awake, but lethargic. Neuro exam is
nonfocal. Labs: Na 121 (last 130 4 weeks ago), normal
renal/liver function. Serum osm 250, urine osm 280,
urine Na 30.
Pretest
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1. What are the potential Causes of
hyponatremia in this patient?
2. Does her urine osm of under 300 rule out
SIADH?
3. What other laboratory data is needed?
4. How might her diet be contributing to her
hyponatremia?
5. How is the urine Na helpful? What in this
case would limit its usefulness?
6. How does water intake or relatively
hypotonic fluid intake worsen hyponatremia
with SIADH?
The Forces Behind Na and
water
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Intracellular volume maintained by regulation of
plasma osmolality (changes in water balance) sensed
by hypothalamic osmoreceptors and affected by ADH
and the thirst mechanism via changes in water intake
and urine osmolality
Plasma volume ultimate goal; maintained by
regulation of Na balance;sensed by afferent arteriole,
carotid sinus, cardiac atria and effected by reninangio-aldo system, sympathetic nervous system, ADH
and atrial natriuretic peptide acting on urine na
excretion
Overview
serum osm (measured)
normal
measure lipids, proteins
volume expanded
CHF
Cirrhosis
nephrotic
low (<280)
Assess ECF Clinically
Volume Depleted
adrenal insuff
extrarenal losses
renal salt wasting
High (>>280)
glucose
mannitol, sorbitol, glycine
Euvolemic
polydipsia
SIADH
Hyponatremia
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Euvolemic
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SIADH
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Relatively high urine
osm (>100, often >300)
High/normal urine Na
(>40)
hypouricemia/urinary
urea wasting
Hypothyroidism
ADH Like compounds
(prolactinoma, HCG,
waldenstrom’s)
Primary Polydipsia
Low urine Osm (<100)
Intake over 10 L/day
Hypovolemic
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appropriate ADH
urine na <20 (unless
diuretic use)
high urine osm (ADH)
hyperuricemia/ dec
urinary uric acid
Hypervolemic
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CHF, cirrhosis, nephrotic
syndrome
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“appropriate ADH”
low urine Na
high urine osm (ADH)
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poor prognostic factor
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ADH
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“antidiuretic”
central role in most all causes of
hyponatremia; must just determined
whether ADH is appropriate, “semi
appropriate”, or inappropriate
Stimulation of release:
nausea/vomiting, pain, volume
depletion
SIADH
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Does not in itself cause edema
(activation of volume receptors leads to
release of urine na and water)
Symptoms relate to rapidity of change
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115-120: headache, lethargy, obtundation
110-115: coma, seizures
SIADH
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Causes:
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CNS: neoplasms, bleed, guillain-barre, SIP,
sarcoidosis (hypothalamic involvement),
pituitary surgery, nausea
Drugs: SSRI, thiazide diuretics,
carbamazepine, haloperidol, amitriptyline,
bromocriptine…
Pneumonia, TB, ARDS, malignancy
Ectopic ADH: carcinomas (small cell),
pancreatic or duodenal ca, thymic ca
ADH like compounds: prolactinoma,
Waldenstrom’s
SIADH: Persistent
Hyponatremia
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Increased ADH> renal
water retention>
increased body water
Body fluid dilution
hyponatremia
dec urine osm over time
with new steady state for
water
hyponatremia persists
until water restricted and
excess water dissipated
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Water intake> renal
water retention >
increased body water
increased ECF volume
increased output, renal
blood flow and decreased
tubular reabsorption of
na (maintain normal
volume!)
increase na excretion
(stretch receptors – inc
natriuretic peptides…)
hyponatremia
new steady state for na
SIADH: Treatment
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Water restriction
Aggressive treatment (3% saline, +/furosemide) not indicated unless
symptomatic, acute, or na <110
no faster than .5 meq/L per hour
correction (to avoid risk of central
pontine myelinolysis)
once na reaches 120, water restriction
only
Volume Depletion
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True volume depletion due to vomiting,
diarrhea, bleeding, urinary losses
n/v also stimulate ADH release (to
maintain circulating volume)
Adrenal Insufficiency (lack of cortisol
resulting in decreased na reabsorption
plus volume depletion)
Volume Depletion: Treatment
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Carefully monitor sodium as fluids given to prevent
overly rapid correction
goal .5 meq/L per hour correction
Degree that 1 L fluid will raise plasma Na conc:
Increase PNa= (infusate [Na] -Pna) / (TBW +1)
Isotonic saline:
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raises plasma sodium by 1-2 meq/L for every liter of fluid
infused since saline has higher Na concentration (154
meq/L) than hyponatremic plasma
volume repletion removes stimulation of ADH
Thiazide Diuretics
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Elderly women at higher risk
Element of volume depletion
Not seen as often with loop diuretics
(inhibition of NaCl transport in loop of Henle
prevents generation of countercurrent
gradient and limits ability of ADH to induce
water retention)
May result in normal/increased urine Na,
even though underlying volume depletion;
CHF, Cirrhosis, Nephrotic
syndrome
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CHF/Cirrhosis: pressure sensed at
carotid sinus baroreceptors reduced due
to poor cardiac output or peripheral
vasodilation/poor circulating volume;
associated with higher mortality; degree
of hyponatremia as prognostic marker
Nephrotic syndrome: usually due to
renal disease rather than poor
circulating volume
Primary Polydipsia
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Psychiatric disorder, often complicated by
increased thirst with antipsychotic meds
can occur with hypothalemic lesions (sarcoid
or other infiltrative processes)
Usually no hyponatremia unless intake over
10-15 L/day, or acute 3-4 L water load
Urine osm below 100 (NOT ADH problem!)
Increased problems if other ADH stimulus
(n/v, anxiety)
Low Dietary Solute Intake
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“Tea and Toast” Diet
Beer drinkers: Beer Potomania
Normally excrete 600-900 mosmol/kg solute
daily (if minimum urine osm is 60 mosmol/kg,
max urine output will be 10-15L/day:
900mosm/day / 60 mosmol/kg = 15)
If daily intake poor, daily solute excretion may
fall below 250 mosmol/kg, reducing the
maximum urine output to below 4 L day;
Hyponatremia develops if greater than 4 L
consumed in day
Urine appears dilute (osm of 100)
Pseudohyponatremia
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Plasma osmolality that is normal or
elevated
usually not at risk for hypoosmolality
induced cerebral edema
Lipids, proteins
Not a problem with labs that directly
measure na
High plasma osmolality
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Hyperglycemia
mannitol
IVIG with maltose retention in patients with
renal failure
Glycine: TURP; exception to rule that patients
with hyperosm hyponatremia do not get into
trouble; complicated by urinary retention, n/v,
postsurgical state; severe hyponatremia after
urological procedure should be treated
acutely with saline/furosemide!
Back to the Case...
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1. What are the potential causes of
hyponatremia in this patient?
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Thiazide diuretic (complicating urine na)
underlying SIADH (suggested by
inappropriately high urine osm)
recent n/v and volume loss (although not
orthostatic)
poor solute intake/ “tea and toast” diet (
may be reason that urine osm is not as high
as would be expected with SIADH alone)
?CNS event (stroke, subdural)
Case...
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2. Does her urine osm of under
300 rule out SIADH?
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No; classically urine osmolality is 300 or
greater, but the urine osm of 220 in the
setting of a serum na of 121 is
inappropriately elevated (over 100 really is
inappropriate)
Case...
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3. What other laboratory data
would be needed?
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TSH
Cortisol level (although not orthostatic)
probably neuroimaging given underlying
dementia and risk for CVA, subdural, etc
consider uric acid to help differentiate
hypovolemia from SIADH (hypouricemia in
SIADH, elevated/normal uric acid if
dehydrated)
Case...
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4. How might her diet be
contributing to her hyponatremia?
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Poor solute intake could result in dilute
urine and hyponatremia as discussed
previously
Case...
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5. How is the urine Na helpful in
differentiating SIADH from
hypovolemia? What in this case
would limit its usefulness?
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Urine Na should be normal/elevated with
SIADH and should be low with
hypovolemia
thiazide diuretic use may elevated urine na
temporarily
Case...
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6. How does water intake or hypotonic fluid intake
worsen the hyponatremia with SIADH?
 Example: patient with SIADH, urine osmolality of 616
mosmol/kg; 1 liter of NS has 308 mosmol of NaCl, 1000 cc
H2O;
 Isotonic Saline
NaCl
H2O
 In
308
1000 ml
 Out
308
500 ml (conc 616)
 Net
0
+500 of free H2O!
Case...
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7. How would you manage this patient?
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Water restriction? Need to address amount of intake
she has had
Avoid rapid correction (osmotic demylination)
Discontinuation of Thiazide
Would probably not give IVF initially as most may be
due to thiazide, SIADH, poor diet, although may be
complicating element of hypovolemia; if n/v
persisted after holding thiazide, consider small
amount of normal saline (relatively hypertonic with
urine osm of 220)