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    HYPERNATRAEMIA

    DEFINITION

    A serum sodium concentration greater than 145 mmol/L (mEq/L).

    TOXIC CAUSES

    Secondary to insufficient water intake
         CNS depression from toxic cause 
         Toxic delirium

    Secondary to excessive water loss
         Cholinergic syndrome with severe sweating 
         Drug-induced nephrogenic diabetes insipidus
              Lithium
              Demeclocycline
         Lactulose 
         Laxatives
         Mannitol
         Severe gastroenteritis from toxic cause

    Secondary to excessive sodium ingestion
         Penicillins (some)
         Sodium Chloride
         Sodium Valproate 

    NON-TOXIC CAUSES

    Diabetes insipidus
    Environmental exposure with dehydration
    Hyperglycaemia leading to osmotic diuresis
    Iatrogenic (hypertonic fluid administration, inadequate free water)
    Interstitial nephritis
    Polyuric phase of renal failure (eg, after relief of prolonged urinary
    obstruction)

    CLINICAL FEATURES

    Delirium and decreased level of consciousness may occur with severe
    hypernatraemia.  Associated illness or circumstances of exposure may
    result in hypovolaemia and hypotension.  Patients with heat exposure
    may also be hyperpyrexic.

    DIFFERENTIAL DIAGNOSIS

    None

    RELEVANT INVESTIGATIONS

    Serum sodium
    Serum potassium, chloride, and bicarbonate
    Renal function tests (urea, creatinine)
    Blood glucose (to exclude hyperglycaemia as a cause of free water
    loss)
    Serum calcium and magnesium
    Urine sodium
    Urine osmolality (This is the most useful test to determine the cause
    of hypernatraemia.  Patients who are dehydrated but with normal renal
    function usually have an elevated urine osmolality [greater than 400
    mOsm/kg].  Patients with impaired ADH secretion or reduced
    responsiveness of the kidney to ADH, will usually have a urine
    osmolality of less than 250 mOsm/kg.)

    TREATMENT

    Use caution, as overly rapid correction of serum sodium can lead to
    cerebral oedema.  The goal of treatment should be to correct the serum
    sodium at a rate no faster than 1 mmol/L/hour or 25 mEq/L/day.  In
    asymptomatic patients, a rate of 0.5 mmol/L/hour is acceptable. 
    Obtain frequent measurements of the serum sodium and adjust treatment
    accordingly. 

    Patients with hypovolaemia should be initially treated with
    intravenous isotonic saline.  Once volume is restored, this should be
    changed to half-normal saline with dextrose.

    Patients with normovolaemic hypernatraemia may be treated with oral
    water administration or intravenous 5% dextrose solution.  Patients
    who are hypervolaemic may need a loop diuretic such as  furosemide to
    remove excess volume. 

    Patients with lithium-induced nephrogenic diabetic insipidus who do
    not improve after discontinuation of lithium may be treated with
     indomethacin, 50 mg every 8 hours, and  hydrochlorothiazide 50 to
    100 mg/day. 

    CLINICAL COURSE AND MONITORING 

    Follow volume status and electrolytes carefully, and avoid overly
    rapid correction of the serum sodium.  Patients should be monitored
    for altered mental status and coma.

    LONG-TERM COMPLICATIONS

    Overly rapid correction of hypernatraemia may cause cerebral oedema
    and permanent brain damage. 

    AUTHOR(S)/REVIEWERS

    Author:        Dr Kent R. Olson, University of California,
                   San Francisco, USA (February 1999).

    Reviewers:     Birmingham 3/99: B Groszek, H Kupferschmidt,
                   N Langford, K Olson, J Pronczuk.