hyponatremia
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Hyponatremia. Debra Bynum,MD Division of Geriatric Medicine. Clinical Case. - PowerPoint PPT PresentationTRANSCRIPT
Hyponatremia
Debra Bynum,MDDivision of Geriatric Medicine
Clinical Case 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 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 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 renin-angio-aldo system, sympathetic nervous system, ADH and atrial natriuretic peptide acting on urine na excretion
Overview
n orm a lm easu re lip id s , p ro te in s
vo lu m e exp an d edC H F
C irrh os isn ep h ro tic
V o lu m e D ep le tedad ren a l in su ff
extra ren a l lossesren a l sa lt w as tin g
E u vo lem icp o lyd ip s ia
S IA D H
low (< 2 8 0 )A ssess E C F C lin ica lly
H ig h (> > 2 8 0 )g lu cose
m an n ito l, so rb ito l, g lyc in e
seru m osm (m easu red )
Hyponatremia Euvolemic
SIADH 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 appropriate ADH urine na <20 (unless
diuretic use) high urine osm (ADH) hyperuricemia/ dec urinary
uric acid Hypervolemic
CHF, cirrhosis, nephrotic syndrome
“appropriate ADH” low urine Na high urine osm (ADH) poor prognostic factor
ADH
“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
Does not in itself cause edema (activation of volume receptors leads to release of urine na and water)
Symptoms relate to rapidity of change 115-120: headache, lethargy, obtundation 110-115: coma, seizures
SIADH Causes:
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 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
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 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
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 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:
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
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 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
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 “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
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 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... 1. What are the potential causes of
hyponatremia in this patient? 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...
2. Does her urine osm of under 300 rule out SIADH? 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... 3. What other laboratory data
would be needed? 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...
4. How might her diet be contributing to her hyponatremia? Poor solute intake could result in
dilute urine and hyponatremia as discussed previously
Case...
5. How is the urine Na helpful in differentiating SIADH from hypovolemia? What in this case would limit its usefulness? Urine Na should be normal/elevated with
SIADH and should be low with hypovolemia
thiazide diuretic use may elevated urine na temporarily
Case... 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... 7. How would you manage this patient?
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)