Hyponatraemia: most patients in severe cases recovered well.

Clinical bottom line (level 4)

  1. Most patients with severe symptomatic hyponatraemia recovered without neurologic sequelae or central pontine demyelination.
Ayus et al: New England Journal of Medicine 1987; 317 (19): 1190-1195
Expires July 2005

The study

Case series with objective outcomes, not adjusted for confounding factors, not validated in an independent set of patients.

Setting: university hospital, USA

33 patients (aged range 42 to 80 years, 61% female) symptomatic hyponatraemia (Na <120 mmol/l); mean Na 108 mmol/l. 36% were in a coma; 61% were lethargic or disorientated
All patients were treated in intensive therapy units, and received 5% hypertonic saline calculated to increase the serum sodium concentration to 120-135 mmol/l. Mean rate of correction 0.83 mmol/l/hr.

100% followed for 5 weeks
Outcomes studied:
  • normal neurologic status
  • central pontine demyelination

    • The evidence

    outcome time to outcome number of patients/total number %
    (95% CI)
    normal neurologic status 5 weeks 33/33 100%
    (91% to 100%)
    central pontine demyelination 5 weeks 0/33 0.0%
    (0.0% to 8.7%)

    • Hyponatraemia was caused by diuretics, SIADH or bladder irrigation. Only three patients developed hyponatraemia in <24 hours.

    Comments

    1. This study reports that demyelination and neurologic consequences are not related to the rate of correction, but it is too small to exclude these outcomes.

    Citation

    1. Ayus JC, Krothapalli RK, Arieff AI: Treatment of symptomatic hyponatremia and its relation to brain damage: a prospective study. New England Journal of Medicine 1987; 317 (19): 1190-1195
    Search Terms: hyponatrem* in Medline
    Contributor: Chris Ball and Clare Wotton, July 2000
    Reviewer:

    Clinical Question.
    Patient symptomatic hyponatraemia
    Intervention or Exposure prevalence
    Outcome brain damage