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Background. Although hyponatraemia [plasma sodium (PNa) <136?mmol/l] frequently develops in hospital, risk factors for hospital-acquired hyponatraemia remain unclear.Methods. Patients who presented with severe hyponatraemia (PNa = 125?mmol/l) were compared with patients with hospital-acquired severe hyponatraemia in a 3 month hospital-wide cohort study.Results. Thirty-eight patients had severe hyponatraemia on admission (PNa 1214?mmol/l), whereas 36 patients had hospital-acquired severe hyponatraemia (PNa 1335 ? 1224?mmol/l). In hospital-acquired hyponatraemia, treatment started significantly later (1.02.6 vs 9.810.6 days, P<0.001) and the duration of hospitalization was longer (18.211.5 vs 30.723.4 days, P = 0.01). The correction of PNa in hospital-acquired hyponatraemia was slower after both 24?h (64 vs 44?mmol/l, P = 0.009) and 48?h (106?mmol/l vs 65?mmol/l, P = 0.001) of treatment. Nineteen patients (26%) from both groups were not treated for hyponatraemia and this was associated with a higher mortality rate (seven out of 19 vs seven out of 55, P = 0.04). Factors that contributed to hospital-acquired hyponatraemia included: thiazide diuretics (none out of 38 vs eight out of 36, P = 0.002), drugs stimulating antidiuretic hormone (two out of 38 vs eight out of 36, P = 0.04), surgery (none out of 38 vs 10 out of 36, P<0.001) and hypotonic intravenous fluids (one out of 38 vs eight out of 36, P = 0.01). Symptomatic hyponatraemia was present in 27 patients (36%), and 14 patients died (19%).Conclusions. The development of severe hyponatraemia in hospitalized patients was associated with treatment-related factors and inadequate management. Early recognition of risk factors and expedited therapy may make hospital-acquired severe hyponatraemia more preventable. [ABSTRACT FROM AUTHOR]

Background. Our objective was to study the risk factors and mechanisms of hypernatraemia in critically ill patients, a common and potentially serious problem. Methods. In 2005, all patients admitted to the medical, surgical or neurological intensive care unit (ICU) of a university hospital were reviewed. A 1:2 matched case-control study was performed, defining cases as patients who developed a serum sodium ≥150 mmol/l in the ICU. Results. One hundred and thirty cases with ICU-acquired hypernatraemia (141 ± 3 to 156 ± 6 mmol/l) were compared to 260 controls. Sepsis (9% versus 2%), hypokalaemia (53% versus 34%), renal dysfunction (53% versus 13%), hypoalbuminaemia (91% versus 55%), the use of mannitol (10% versus 1%) and use of sodium bicarbonate (23% versus 0.4%) were more common in cases (P < 0.05 for all) and were independently associated with hypernatraemia. During the development of hypernatraemia, fluid balance was negative in 80 cases (−31 ± 2 ml/kg/day), but positive in 50 cases (72 ± 3 ml/kg/day). Cases with a positive fluid balance received more sodium plus potassium (148 ± 2 versus 133 ± 3 mmol/l, P < 0.001). On average, cases were polyuric (40 ± 5 ml/kg). Mortality was higher in cases (48% versus 10%, P < 0.001), for which hypernatraemia was an independent predictor (odds ratio 4.3, 95% confidence interval 2.5 to 7.2). Conclusions. Hypernatraemia seems to develop in the ICU because various factors promote renal water loss, which is then corrected with too little water or overcorrected with relatively hypertonic fluids. Therapy should therefore rely on adding electrolyte-free water and/or creating a negative sodium balance. Adjustments in intravenous fluid regimens may prevent hypernatraemia. [ABSTRACT FROM AUTHOR]

Background. The objective was to study the epidemiology of hypokalaemia [serum potassium concentration (SK) SK ≥5.0 mmol/l). Methods. In a 3-month hospital-wide study we analysed factors contributing to hypokalaemia and subsequent hyperkalaemia. Results. From 1178 patients in whom SK was measured, 140 patients (12%) with hypokalaemia were identified (SK 3.0 ± 0.3 mmol/l). One hundred patients (71%) had hospital-acquired hypokalaemia. Common causes of hypokalaemia included gastrointestinal losses (67%), diuretics (36%) and haematological malignancies (9%). In 104 patients (74%), hypokalaemia was multifactorial. Hypokalaemia frequently coexisted with hyponatraemia (24%) and, when measured, hypomagnesaemia (61%). Twenty-three patients (16%) developed hyperkalaemia (highest SK 5.7 ± 0.7 mmol/l) following hypokalaemia. In these patients, potassium suppletion was not more common (70 vs 59%, P = 0.5), but when potassium was given, the total amount administered was significantly higher (median 350 mmol vs 180 mmol, P = 0.02). Furthermore, these patients more often received total parenteral nutrition (17 vs 4%, P = 0.02) and magnesium suppletion (30 vs 9%, P = 0.009), and more often had haematological malignancies (22 vs 6%, P = 0.03). Conclusions. Hypokalaemia is a multifactorial and usually hospital-acquired condition associated with hyponatraemia and hypomagnesaemia. One out of every six patients with hypokalaemia developed subsequent hyperkalaemia. Besides potassium suppletion, total parenteral nutrition (source of potassium), magnesium suppletion (may reduce kaliuresis) and haematological malignancy (may cause cell lysis) contribute to hyperkalaemia following hypokalaemia. Caution with potassium suppletion and frequent monitoring of SK may prevent iatrogenic hyperkalaemia. [ABSTRACT FROM AUTHOR]