Evaluation and Management of Hyponatremia in the Elderly (PowerPoint)

Document Sample
Evaluation and Management of Hyponatremia in the Elderly (PowerPoint) Powered By Docstoc

         Debra Bynum,MD
   Division 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.
   1. What are the potential Causes of
    hyponatremia in this patient?
   2. Does her urine osm of under 300 rule out
   3. What other laboratory data is needed?
   4. How might her diet be contributing to her
   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
   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
   Euvolemic                            Hypovolemic
       SIADH                                appropriate ADH
             Relatively high urine
                                             urine na <20 (unless
             osm (>100, often >300)
                                              diuretic use)
            High/normal urine Na
             (>40)                           high urine osm (ADH)
            hypouricemia/urinary            hyperuricemia/ dec
             urea wasting                     urinary uric acid
       Hypothyroidism                   Hypervolemic
       ADH Like compounds                   CHF, cirrhosis, nephrotic
        (prolactinoma, HCG,                   syndrome
        waldenstrom’s)                            “appropriate ADH”
       Primary Polydipsia                        low urine Na
            Low urine Osm (<100)                 high urine osm (ADH)
            Intake over 10 L/day                 poor prognostic factor
   “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
   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
   Causes:
       CNS: neoplasms, bleed, guillain-barre, SIP,
        sarcoidosis (hypothalamic involvement),
        pituitary surgery, nausea
       Drugs: SSRI, thiazide diuretics,
        carbamazepine, haloperidol, amitriptyline,
       Pneumonia, TB, ARDS, malignancy
       Ectopic ADH: carcinomas (small cell),
        pancreatic or duodenal ca, thymic ca
       ADH like compounds: prolactinoma,
SIADH: Persistent
   Increased ADH> renal            Water intake> renal
    water retention>                 water retention >
    increased body water             increased body water
   Body fluid dilution             increased ECF volume
   hyponatremia                    increased output, renal
   dec urine osm over time          blood flow and decreased
    with new steady state for        tubular reabsorption of
    water                            na (maintain normal
    hyponatremia persists           increase na excretion
    until water restricted and       (stretch receptors – inc
    excess water dissipated          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
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
   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)
   Plasma osmolality that is normal or
   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
       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)
   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
   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
   4. How might her diet be
    contributing to her hyponatremia?
       Poor solute intake could result in dilute
        urine and hyponatremia as discussed
   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
       thiazide diuretic use may elevated urine na
   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
         Isotonic Saline    NaCl      H2O
         In                   308       1000 ml
         Out          308          500 ml (conc 616)
         Net                    0          +500 of free H2O!
   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)