Estimation of sodium and chloride storage in critically ill patients: a balance study

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.Electronic supplementary materialThe online version of this article (10.1186/s13613-018-0442-2) contains supplementary material, which is available to authorized users.

ICU acquired hypernatremia treated by enteral free water – A retrospective cohort study

“…IAH may be a sign of severity of disease, which is supported by the significantly higher 'highest' SOFA score in the non-responders. Also accumulating evidence on a more complex sodium homeostasis irrespective of volume status disturbs the old view on too much salt or too little water even more [18][19][20].…”

“…The sodium homeostasis in critically ill patients however, could be more complex than previously thought. Recent literature has shown that IAH is not explained by sodium overload or water deficit and there is evidence of non-osmotic sodium storage in the muscles and skin [18][19][20]. Nevertheless, it is unclear whether the addition of enteral free water is effective in a complex homeostatic system of sodium regulation in critically ill patients.…”

Intensive Care Unit Acquired Hypernatremia after Major Surgery is Associated with Urine Concentrating Defect: An Observational Study

“…We have to question to what extent balances are at all able to explain changes in sodium concentration [16]. There is evidence that sodium is stored non-osmotically in critically ill patients [17]. Moreover, there are always inaccuracies in the balance due to factors with unknown quantity or unknown sodium concentration like perspiration, gastric juice, stool or internal bleeding.…”