To observe the incidence of complications in severely hyponatraemic hospitalized patients and relate outcome to rate of correction, all patients admitted to a tertiary referral hospital in New York City, USA or a group of hospitals in Oxford, UK with a sodium ≤120 mmol/l were studied. Review of the notes and prospective evaluation were used to ascertain cause of hyponatraemia, method of management and outcome. There were 84 episodes in New York and 100 in Oxford, over 9.5 months and one year, respectively; 79 had chronic hyponatraemia ( > 3 days duration). During hyponatraemia, 76 of patients had clouding of consciousness with 11 in coma. Other hyponatraemic complications included long track signs (including hemipar-esis) (6.0), seizures (3.3), hallucinations (0.5), tremor (1.0), intellectual impairment without clouding of consciousness (0.5), and acute psychosis (0.5). 4.3 died as a direct result of their electrolyte disturbance. After correction, central pontine myelinolysis (0.5), post-correction seizures (1.0), intellectual impairment (2.2), tremor (0.5), paraesthesiae (0.5), and striatal syndrome (0.5) were observed. Correction of hyponatraemia was started in 158 patients, and the mean maximum rate of correction in 24 h was 8.4 mmol/l (SD 5.6, range 2-42). The maximum rate of correction was higher in those who developed neurological sequelae (12.1 mmol/l/24 h vs. 8.2 mmol/l/24 h; p=0.0125, t-test, separate variance, two-tail). Neurological sequelae were associated with faster rates of correction, and correction of chronic severe hyponatraemia should be < 10 mmol/l in 24 h.
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