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Clinical Features of Hyponatraemia:



  • Manifestations of hyponatraemia depend greatly on the rate of its
    development. A very slowly progressive hyponatraemia can be
    asymptomatic while acutely developing hyponatraemia could be
    very serious.

  • With hyponatraemia, plasma will be hypotonic while cells
    (especially brain cells) will be hypertonic. To achieve osmotic
    equilibrium, water will move from plasma to cells with a consequent
    cell oedema (brain oedema).

  • Plasma sodium concentrations above 120 mmol/L are usually well
    tolerated, while the majority of patients will have severe cerebral
    dysfunction once plasma sodium is below 110 mmol/L (lethargy,
    anorexia, nausea, vomiting, confusion, disorientation, convulsions,
    coma and even permanent brain damage).


Treatment of Hyponatraemia:



  • In severe hyponatraemia, rapid correction with hypertonic saline is
    contraindicated as it may lead to fatal central pontine myelinolysis. It
    is wise to increase plasma sodium by only 5-10 mmol/Litre per 24
    hours. This is achieved through the administration of loop-diuretic
    and normal saline and in severe cases, small amounts (100-200 ml)
    of hypertonic (double strength i.e. 300 mmol/L) saline may be
    infused.

  • Correction of the underlying cause, in the overloaded patient water
    restriction can be combined with loop-diuretics as furosemide and
    sometimes salt supplements.

  • In SIADH, lithium or demeclocycline may be given to induce a renal
    concentration defect.

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