Catabolism highly influences ICU-acquired hypernatremia in a mainly trauma and surgical cohort.

To further analyse causes and effects of ICU-acquired hypernatremia. This retrospective, single-centre study, analysed 994 patients regarding ICU-acquired hypernatremia. Non-hypernatremic patients (n = 617) were compared to early-hypernatremic (only before ICU-day 4; n = 87), prolonged-hypernatremic (before and after ICU-day 4; n = 169) and late-hypernatremic patients (only after ICU-day 4; n = 121). Trends in glomerular filtration rate (eGFR), urea-to-creatinine ratio (UCR), fraction of urea in total urine osmolality and urine sodium were compared. Risk factors for i) the development of hypernatremia and ii) mortality were determined. Thirty-eight percent (n = 377) developed ICU-acquired hypernatremia. Specifically in the prolonged- and late-group, decreased eGFRs and urine sodium but increased UCR and fractions of urea in urine osmolality were present. Decreased eGFR was a risk factor for the development of hypernatremia in all groups; disease severity and increased catabolism particularly in the prolonged- and late-hypernatremic group. Increased age, SAPS-III and signs of catabolism but not the development of hypernatremia itself was identified as significant risk factor for mortality. Late- and prolonged-hypernatremia is highly related to an increased protein metabolism. Besides excessive catabolism, initial disease severity and a decrease in renal function must be considered when confronted with ICU-acquired hypernatremia.

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