Background: Hospital-acquired hyponatraemia is a common and potentially serious condition. Risk factors for hospital-acquired hyponatraemia have not been studied in a controlled fashion. Methods From 1501 patients in whom serum sodium (S(Na)) was determined, 50 cases with hospital-acquired hyponatraemia (in-hospital decrease in S(Na)>or= 7 mmol/l to < 136 mmol/l) were identified. They were matched by age, gender and department to 69 normonatraemic controls.
Results: In the 50 cases, S(Na) fell from 141 +/- 2 to 130 +/- 4 mmol/l, while controls remained normonatraemic. During the development of hyponatraemia, C-reactive protein (CRP) increased in cases (median from 23 to 146 mg/l), whereas it decreased in controls (median from 31 to 24 mg/l, P = 0.008). Additional factors associated with hospital-acquired hyponatraemia included diabetes mellitus (16/50 vs. 10/69, P = 0.009) and the use of insulin (12/50 vs. 4/69, P = 0.007), antibiotics (41/50 vs. 38/69, P = 0.006) and opioids (32/50 vs. 27/69, P = 0.005). Multivariate conditional logistic regression showed that the use of insulin [odds ratio (OR) 10.5, 95% confidence interval (CI) 1.5-72.4], antibiotics (OR 4.5, 95% CI 1.4-14.6) and opioids (OR 2.9, 95% CI 1.1-7.8) was also independently associated with hospital-acquired hyponatraemia. Mortality (6/50 vs. 1/69, P = 0.04) and intensive care admission (15/50 vs. 7/69, P = 0.008) were higher in cases.
Conclusions: An increase in CRP and the use of insulin, antibiotics and opioids are novel risk factors for hospital-acquired hyponatraemia. These factors represent interesting new clues regarding the pathophysiology of hospital-acquired hyponatraemia, suggesting that the acute-phase response, pain and/or direct drug effects could be involved in the release of antidiuretic hormone.