HYPONATRAEMIA

    DEFINITION

    A serum sodium concentration of less than 135 mmol/L (mEq/L). 

    TOXIC CAUSES 

    Secondary to excessive water intake
         Excessive oral fluids
         Hypotonic intravenous fluids 

    Secondary to excessive sodium loss
         Diuretics
         Drug-associated Syndrome of Inappropriate Antidiuretic Hormone
           secretion (SIADH)
              Amitriptyline and other tricyclic antidepressants
              Carbamazepine 
              Chlorpropamide and Tolbutamide
              Clofibrate 
              Cyclophosphamide and Vincristine 
              Fluoxetine
              Monoamine oxidase inhibitors
              Nonsteroidal anti-inflammatory drugs (NSAIDs)
              Oxytocin 
              Phenothiazines 
              Somatostatin 
              Thiothixene

    NON-TOXIC CAUSES 

    Congestive heart failure
    Diarrhoea
    Hypothyroidism
    Liver disease
    Mineralocorticoid deficiency (Addison's Disease)
    Nephropathy
    Psychogenic polydipsia
    Postoperative hyponatraemia
    Rehydration with hypotonic fluids
    SIADH from non-toxic causes
         AIDS 
         Carcinomas
         CNS disorders
         Postoperative pain or stress
         Pulmonary infections and lesions
         Vomiting

    CLINICAL FEATURES 

    Patients with hyponatraemia may be lethargic or confused.  Seizures
    and coma may occur with very low serum sodium concentrations (less
    than 110 to 120 mmol/L), especially where concentrations fall rapidly. 
    Hyponatraemia that develops more slowly may be better tolerated. 

    DIFFERENTIAL DIAGNOSIS

    Pseudohyponatraemia may be produced by a shift of water from the
    extracellular to the intracellular space.  This can result from
    hyperlipidaemia or hyperglycaemia.

    RELEVANT INVESTIGATIONS 

    Serum sodium
    Serum potassium, chloride, and bicarbonate
    Renal function tests (urea, creatinine)
    Glucose (to exclude hyperglycaemia as a cause of pseudohyponatraemia)
    Liver function tests
    Serum calcium, magnesium
    Urine sodium
    Urine osmolality (The most useful tests to determine the cause of
    hyponatraemia are the urine sodium and urine osmolality.  SIADH is
    associated with inappropriately high urine osmolality.  Elevated urine
    sodium concentrations suggest renal salt wasting, which can be due to
    diuretic use or nephropathy.  A low urine sodium concentration and low
    urine osmolality suggest excessive free water intake.)
    Serum osmolality, albumin, triglycerides (to exclude
    pseudohyponatraemia)

    TREATMENT

    Treatment should be instituted with caution because overly rapid
    correction of hypernatraemia may lead to brain damage (central pontine
    myelolysis).  The aim of treatment should be to increase the serum
    sodium concentration at a rate no faster than 1 mmol/L/hour or 25
    mmol/L/day.  In asymptomatic patients, 0.5 mmol/L/hour is adequate. 
    Obtain frequent measurements of the serum sodium concentration and
    adjust treatment accordingly. 

    Patients who are hypovolaemic may be treated with normal saline. 
    Normovolaemic patients are usually treated with water restriction (0.5
    to 1 L/day).  Patients with volume overload (e.g. congestive cardiac
    failure) may be treated with a combination of fluid restriction and
    diuretics. Haemodialysis may be needed for patients with renal
    failure. 

    SIADH may respond to discontinuation of the offending drug. 
     Demeclocycline may be required for severe or non-responsive cases. 

    Only those patients with profound hyponatraemia (<110 mEq/L)
    accompanied by seizures or coma should be treated more rapidly with
    hypertonic saline (3% saline, 100 to 200 mL intravenously over 30
    minutes). 

    CLINICAL COURSE AND MONITORING 

    Monitor volume status and electrolytes carefully, and avoid overly
    rapid correction of the serum sodium concentration.  Patients should
    be monitored for seizures. 

    LONG-TERM COMPLICATIONS 

    Severe hyponatraemia, or overly rapid correction of hyponatraemia, may
    cause permanent CNS injury.

    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.