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Physiology of Hyponatremia

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2. CHF, cirrhosis (effective volume depletion) 3. Diuretic use. 4. Adrenal insufficiency ... for hyponatremia in edematous states (CHF, cirrhosis) and in SIADH ... – PowerPoint PPT presentation

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Title: Physiology of Hyponatremia


1
Physiology of Hyponatremia
  • Hyponatremia results from either the excessive
    intake or inability to excrete free water.
  • Water intake?dilutional fall in plasma
    osmolality? suppression of ADH.
  • Plasma osmolality is elevated OR effective
    circulating volume is low?ADH secretion
  • Normals can excrete over 10 L of free water a day.

2
Differential Diagnosis
  • Conditions in which ADH levels are elevated
  • 1. Volume depletion (vomiting, diarrhea,
    hemorrhage, profuse sweating)
  • 2. CHF, cirrhosis (effective volume depletion)
  • 3. Diuretic use
  • 4. Adrenal insufficiency
  • 5. SIADH

3
Differential Diagnosis
  • Conditions in which ADH levels are suppressed
  • 1. Advanced renal failure
  • 2. Primary polydipsia
  • 3. Low dietary solute intake
  • 4. Beer potomania
  • Pseudohyponatremiarare
  • 1. High Sosms hyperglycemia, mannitol
  • 2. Normal Sosms hyperlipidemia,
    hyperproteinemia

4
Workup
  • History and PE are focused on volume status
  • Later on, pattern recognition helps
  • The elderly lady on a tea and toast diet who is
    also taking a diuretic
  • The cirrhotic with worsening ascites, edema
  • Early on, be complete with the evaluation send
    UA (specific gravity is the poor mans Sosm)
    serum osmolality, urine osmolality, urine
    electrolytes
  • Urine electrolytes give another assessment of
    volume status (Na should be lt10 in volume
    depletion, unless on diuretic), K handling

5
Workup
  • A normal or elevated Uosm (above 100) in the
    setting of low Posms makes the diagnosis of
    SIADH.
  • --usually Na is gt40
  • --usually Creatinine is normal
  • --normal acid-base, K handling
  • Low Uosm (less than 100) seen in primary
    polydipsia, poor solute intake

6
Workup
  • Distinguishing hypovolemia/diuretic induced from
    SIADH (or presence of both)
  • --Urine Na usually low
  • --PE reveals signs dehydration
  • --Creatinine may be elevated
  • --hold diuretic and hydrate if the Urine Na
    rises to above 40 and the Uosms remain above 100
    the patient also has SIADH.

7
Treatment
  • Goal to prevent cerebral edema and
    encephalopathy (lethargy, obtundation, seizures,
    coma, arrest) while preventing central pontine
    myelinolysis (correcting sodium too rapidly.)
  • More rapid therapy (1.5 to 2 mEq per hour) can be
    used in the first few hours if there is serious
    cerebral dysfunction. Otherwise, maximum rate of
    elevation 10-12 mEq during the first 24 hours
    and 18 mEq/L in the first two days.

8
Ways to Raise Serum Sodium
  • Water restrictionchronic primary therapy for
    hyponatremia in edematous states (CHF, cirrhosis)
    and in SIADH
  • SIADH in the acute setting must be treated with
    IVF that exceeds the Uosm (NS or hypertonic
    saline)
  • In volume depletionuse normal saline

9
Calculation of the Sodium Deficit
  • TBW times the net sodium gain
  • 0.5 times the weight in kilos for women, 0.6 for
    men
  • Example of 50 kg female, sodium of 122
  • So, if we wish her sodium to be raised by 12 mEq
    in the first 24 hours
  • --0.5 x 50 kg x 12 300 mEq
  • Hypertonic saline contains roughly 1 mEq of
    sodium per 2 cc, so 600 cc should be given over
    24 hours (25 cc/hour)

10
Ddx of SIADH
  • CNS head trauma, neurosurgery, psychiatric
    illness, stroke, infection
  • Tumor ectopic ADH due to small cell Ca of the
    lung (most common), also seen in bronchogenic Ca,
    pancreatic Ca, neuroblastoma (rarer)
  • Drugs Carbamazepine, chlorpropamide, highdose
    IV cyclophosphamide, SSRIs
  • Major surgery
  • Pulmonary disease (particularly pneumonia)
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