Abstract
BackgroundNonosmotic sodium storage has been reported in animals, healthy individuals and patients with hypertension, hyperaldosteronism and end-stage kidney disease. Sodium storage has not been studied in ICU patients, who frequently receive large amounts of sodium chloride-containing fluids. The objective of our study was to estimate sodium that cannot be accounted for by balance studies in critically ill patients. Chloride was also studied. We used multiple scenarios and assumptions for estimating sodium and chloride balances.MethodsWe retrospectively analyzed patients admitted to the ICU after cardiothoracic surgery with complete fluid, sodium and chloride balance data for the first 4 days of ICU treatment. Balances were obtained from meticulously recorded data on intake and output. Missing extracellular osmotically active sodium (MES) was calculated by subtracting the expected change in plasma sodium from the observed change in plasma sodium derived from balance data. The same method was used to calculate missing chloride (MEC). To address considerable uncertainties on the estimated extracellular volume (ECV) and perspiration rate, various scenarios were used in which the size of the ECV and perspiration were varied.ResultsA total of 38 patients with 152 consecutive ICU days were analyzed. In our default scenario, we could not account for 296 ± 35 mmol of MES in the first four ICU days. The range of observed MES in the five scenarios varied from 111 ± 27 to 566 ± 41 mmol (P < 0.001). A cumulative value of 243 ± 46 mmol was calculated for MEC in the default scenario. The range of cumulative MEC was between 62 ± 27 and 471 ± 56 mmol (P = 0.001 and P = 0.003). MES minus MEC varied from 1 ± 51 to 123 ± 33 mmol in the five scenarios.ConclusionsOur study suggests considerable disappearance of osmotically active sodium in critically ill patients and is the first to also suggest rather similar disappearance of chloride from the extracellular space. Various scenarios for insensible water loss and estimated size for the ECV resulted in considerable MES and MEC, although these estimates showed a large variation. The mechanisms and the tissue compartments responsible for this phenomenon require further investigation.
Highlights
Nonosmotic sodium storage has been reported in animals, healthy individuals and patients with hypertension, hyperaldosteronism and end-stage kidney disease
Patients admitted to the intensive care unit (ICU) typically receive large amounts of sodium and chloride during their ICU treatment [8]
Missing extracellular osmotically active sodium and chloride Based on our calculations, for sodium a MES of 74 ± 15 mmol per day was observed
Summary
Nonosmotic sodium storage has been reported in animals, healthy individuals and patients with hypertension, hyperaldosteronism and end-stage kidney disease. When long-term balance studies in humans demonstrated that sodium could accumulate without weight gain or hypernatremia, this challenged the generally accepted model on sodium homeostasis [1] This model states that changes in sodium homeostasis can primarily be explained by a two-compartment model with an Hessels et al Ann. Intensive Care (2018) 8:97 suggested in animal models [6, 7], but has not been as extensively studied as sodium storage. Patients admitted to the intensive care unit (ICU) typically receive large amounts of sodium and chloride during their ICU treatment [8] Both hypernatremia and hyperchloremia are a frequent complication in critically ill patients and are associated with adverse outcome [9,10,11,12]. A potentially similar phenomenon for chloride has not been studied yet
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