ICU-acquired Hypernatremia Research Articles

Enteral free water vs. parenteral dextrose 5% in water for the treatment of hypernatremia in the intensive care unit: a retrospective cohort study from a mixed ICU.

Effective treatment options for patients with hypernatremia are limited. Free water administration (parenterally or enterally) is the mainstay of treatment but the impact of each strategy on lowering serum sodium (Na) is not known.The purpose of the study was thus toassess the effectiveness of enteral free water vs. parenteral dextrose 5% in water (D5W) in treating ICU-acquired hypernatremia. An electronic medical record-based, retrospective cohort study was conducted in a 30-bed mixed medical-surgical intensive care unit (ICU) in Japan. All adult patients admitted to the ICU from August 2017 to July 2021 were reviewed. After a 2-step exclusion, patients who stayed in the ICU ≥ 24h and received either or both treatments for ICU-acquired hypernatremia (Na ≥ 145mEq/L) constituted the study cohort. The primary outcome was a change in serum Na during the 24h before treatment each day (ΔNa); the secondary outcomes were gastrointestinal complications, serum glucose levels, ICU/hospital mortality, ICU/hospital length of stay, and the duration of mechanical ventilation. Repeated measurements on each patient were addressed using a generalized estimated equation (GEE) for multiple linear regression analysis. Analysis was conducted with R version 4.0.3. In total, 256/6596 (131: D5W, 125: enteral free water) patients were analyzed. Median treatment lasted 6days [3-17] for the D5W group vs 7days [3-14] for the enteral free water group with a total median daily treatment volume of 799 [IQR 299-1221] mL vs. 400 [IQR 262-573] mL. GEE multiple linear regression analysis showed an estimated mean ΔNa per liter of treatment fluid of - 2.25 [95% CI - 2.76 to - 1.74] mEq/L per liter of parenteral D5W vs. - 1.91mEq decrease [95% CI - 2.75 to - 1.07] per liter of enteral free water. Hydrochlorothiazide was the only medication associated with a statistically significant negative ΔNa by- 0.89 [- 1.57 to - 0.21] mEq/L. There were no significant inter-group differences for secondary outcomes. These results suggest that both enteral free water and parenteral D5W are effective for treating ICU-acquired hypernatremia. Parenteral D5W was slightly more effective than enteral free water to lower serum Na levels in patients with ICU-acquired hypernatremia. Not applicable.

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

PurposeTo further analyse causes and effects of ICU-acquired hypernatremia. MethodsThis 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. ResultsThirty-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. ConclusionsLate- 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.

Association of Hypernatremia with Immune Profiles and Clinical Outcomes in Adult Intensive Care Unit Patients with Sepsis.

Both hypernatremia and an abnormal immune response may increase hospital mortality in patients with sepsis. This study examined the association of hypernatremia with abnormal immune response and mortality in 520 adult patients with sepsis in an intensive care unit (ICU). We compared the mortality and ex vivo lipopolysaccharide (LPS)-induced inflammatory response differences among patients with hyponatremia, eunatremia, and hypernatremia, as well as between patients with acquired hypernatremia on ICU day 3 and those with sustained eunatremia over first three ICU days. Compared with eunatremia or hyponatremia, hypernatremia led to higher 7 day, 14 day, 28 day, and hospital mortality rates (p = 0.030, 0.009, 0.010, and 0.033, respectively). Compared with sustained eunatremia, acquired hypernatremia led to higher 7, 14, and 28 day mortality rates (p = 0.019, 0.042, and 0.028, respectively). The acquired hypernatremia group nonsignificantly trended toward increased hospital mortality (p = 0.056). Day 1 granulocyte colony-stimulating factor (G-CSF) and tumor necrosis factor (TNF) α levels were relatively low in patients with hypernatremia (p = 0.020 and 0.010, respectively) but relatively high in patients with acquired hypernatremia (p = 0.049 and 0.009, respectively). Thus, in ICU-admitted septic patients, hypernatremia on admission and in ICU-acquired hypernatremia were both associated with higher mortality. The higher mortality in patients with hypernatremia on admission was possibly related to the downregulation of G-CSF and TNF-α secretion after endotoxin stimulation. Compared to sustained eunatremia, acquired hypernatremia showed immunoparalysis at first and then hyperinflammation on day 3.

Hypernatremia at a Tertiary Hospital Intensive Care Unit in South Africa.

BackgroundHypernatremia in the critical care setting is a major cause of morbidity and mortality. However, data pertaining to this has not been evaluated in South African hospitals. The aim of this study was to evaluate hypernatremia with regards to its prevalence, associated factors, and outcomes at an academic hospital intensive care unit (ICU) in Johannesburg, South Africa.MethodsThe ICU charts of patients admitted to the Charlotte Maxeke Johannesburg Academic Hospital adult general ICU from June 1, 2016 to May 31, 2017 were retrospectively reviewed. Subjects were categorized into three groups namely, ICU-acquired hypernatremia (IAH), pre-admission hypernatremia (PAH), and normonatremia. Data was compared between the three groups.ResultsOf the 833 subjects that were enrolled, 310 (37.2%) were hypernatremic. IAH was present in 144 (17.2%) and PAH in 166 (19.9%) subjects. Hypernatremia was significantly (p <0.05) associated with a higher rate of altered mental status, higher Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II) scores, a higher rate and duration of mechanical ventilation, a greater need for inotropic/vasopressor support, longer ICU stay and higher ICU mortality.ConclusionHypernatremia in ICU patients remains a significant contributor to morbidity, mortality, and ICU length of stay. The prevalence of hypernatremia was much higher than that reported in higher-income countries.

Increased sodium intake and decreased sodium excretion in ICU-acquired hypernatremia: A prospective cohort study.

To provide more in-depth insight in the development of early ICU-acquired hypernatremia in critically ill patients based on detailed, longitudinal and quantitative data. A comparative analysis was performed using prospectively collected data of ICU patients. All patients requiring ICU admission for more than 48h between April and December 2018 were included. For this study, urine samples were collected daily and analyzed for electrolytes and osmolality. Additionally, plasma osmolality analyses were performed. Further data collection consisted of routine laboratory results, detailed fluid balances and medication use. A total of 183 patient were included for analysis, of whom 38% developed ICU-acquired hypernatremia. Whereas the hypernatremic group was similar to the non-hypernatremic group at baseline and during the first days, hypernatremic patients had a significantly higher sodium intake on day 2 to 5, a lower urine sodium concentration on day 3 and 4 and a worse kidney function (plasma creatinine 251 versus 71.9μmol/L on day 5). Additionally, hypernatremic patients had higher APACHE IV scores (67 versus 49, p<0.05) and higher ICU (23 versus 12%, p=0.07) and 90-day mortality (33 versus 14%, p<0.01). Longitudinal analysis shows that the development of early ICU-acquired hypernatremia is preceded by increased sodium intake, decreased renal function and decreased sodium excretion.

Association Between ICU-Acquired Hypernatremia and In-Hospital Mortality: Data From the Medical Information Mart for Intensive Care III and the Electronic ICU Collaborative Research Database.

Describe the relationship between ICU-acquired hypernatremia and in-hospital mortality and investigate the optimal hypernatremia correction rate. Observational study including two individual ICU cohorts. We used the Medical Information Mart for Intensive Care III v. 1.4 database consists of all ICU patients admitted to the Beth Israel Deaconess Medical Center in Boston from 2001 to 2012 (n = 46,476). The electronic ICU v. 2.0 database consists of all ICU patients admitted to 208 distinct hospitals across the United States from 2014 to 2015 (n = 200,859). We included all adult patients admitted to an ICU with two consecutive sodium samples within normal range (135-145 mmol/L) and without two consecutive hyponatremic samples (< 135 mmol/L) during the ICU stay. Of 23,445 patients identified in Medical Information Mart for Intensive Care III, 9% (n = 2,172) developed hypernatremia during their ICU stay. In electronic ICU, 88,160 patients were identified and 7% (n = 5,790) developed hypernatremia. In both cohorts, patients with hypernatremia had a higher mortality (Medical Information Mart for Intensive Care III: 20% vs 42%; p < 0.01 and electronic ICU: 6% vs 22%; p < 0.01), with hypernatremia increasing the risk of in-hospital mortality (Medical Information Mart for Intensive Care III: odds ratio, 1.15; 95% CI, 1.13-1.17 and electronic ICU: odds ratio, 1.11; 95% CI, 1.10-1.12) and over time using a Cox regression. Rapid sodium correction rate (> 0.5 mmol/L/hr) was associated with an increased in-hospital mortality in both cohorts (Medical Information Mart for Intensive Care III: odds ratio, 1.08; 95% CI, 1.03-1.13 and electronic ICU: odds ratio, 1.10; 95% CI, 1.06-1.13). In the electronic ICU cohort, rapid correction rates were associated with a significant difference in in-hospital mortality, but there was no statistically significant association in the Medical Information Mart for Intensive Care III cohort. ICU-acquired hypernatremia is associated with increased in-hospital mortality. Furthermore, a rapid sodium correction rates may be harmful. This suggests it is important to both prevent ICU-acquired hypernatremia and to avoid rapid correction rates if a patient becomes hypernatremic.

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

ICU acquired hypernatremia (IAH) is associated with increased morbidity and mortality, however treatment remains controversial. This study aims to determine the effect of enteral free water suppletion in patients with IAH. Retrospective single center study in a tertiary ICU. patients with IAH and treatment with enteral free water. patients with renal replacement therapy, diabetic ketoacidosis or hyperosmolar hyperglycaemic state. change in plasma sodium (in mmol/l) after 5days treatment. Responders were defined as patients with a decrease in sodium level of 5mmol/l or more. In total 382 consecutive patients were included. The median sodium level at the start of water therapy was 149mmol/l (IQR 147-150). The median volume of enteral water was 4423ml (IQR 3349-5379ml) after 5days and mean sodium decrease was 1.87mmol/l (SD 4.84). There was no significant correlation between the volume of enteral water and sodium decrease (r2=0.01). Treatment with enteral free water did not result in a clinically relevant decrease in serum sodium level in patients with IAH. In addition, the volume of enteral free water and the use of diuretics was unrelated with sodium change over 5days.

Renal Function is a Major Determinant of ICU-acquired Hypernatremia: A Balance Study on Sodium Handling.

Background and ObjectivesThe development of ICU-acquired hypernatremia (IAH) is almost exclusively attributed to ‘too much salt and too little water’. However, intrinsic mechanisms also have been suggested to play a role. To identify the determinants of IAH, we designed a prospective controlled study.MethodsPatients with an anticipated length of stay ICU > 48 hours were included. Patients with hypernatremia on admission and/or on renal replacement therapy were excluded. Patients without IAH were compared with patients with borderline hypernatremia (≥ 143 mmol/L, IAH 143) and more severe hypernatremia (≥ 145 mmol/L, IAH 145).ResultsWe included 89 patients, of which 51% developed IAH 143 and 29% IAH 145. Sodium intake was high in all patients. Fluid balances were slightly positive and comparable between the groups. Patients with IAH 145 were more severely ill on admission, and during admission, their sodium intake, cumulative sodium balances, serum creatinine and copeptin levels were higher. According to the free water clearance, all the patients conserved water. On multivariate analysis, the baseline serum creatinine was an independent risk factor for the development of IAH 143 and IAH 145. Also, the copeptin levels remained significant for IAH 143 and IAH 145. Sodium intake remained only significant for patients with IAH 145.ConclusionsOur data support the hypothesis that IAH is due to the combination of higher sodium intake and a urinary concentration deficit, as a manifestation of the renal impairment elicited by severe illness.

Glucocorticoid treatment is associated with ICU-acquired hypernatremia: a nested case-control study.

BackgroundHypernatremia is a major electrolyte disorder associated with death among critically ill patients. Glucocorticoid therapy may cause hypernatremia in refractory septic shock patients, but the association between glucocorticoid and intensive care unit (ICU)-acquired hypernatremia (IAH) remains unclear. The aim of this study was to clarify whether glucocorticoid administration was associated with IAH.MethodsThis was a nested case–control study using data from an established cohort including 121 IAH cases identified from 1756 patients who were admitted to ICU in a tertiary care facility in Japan. We included patients who were admitted with a normal range of serum sodium concentrations (130–149 mEq/L) from January 1, 2013 to December 31, 2015 and remained in ICU for ≥ 2 days. Hypernatremia was defined as serum sodium concentration ≥ 150 mEq/L. Each case was matched to one control.ResultsMultivariable conditional logistic regression revealed high-dose glucocorticoid {odds ratio (OR), 4.15 [95% confidence interval (CI) 1.29–13.4]}, acute kidney injury (AKI) [OR, 2.72 (95% CI 1.31–5.62)], and osmotic diuretics [OR, 3.44 (95% CI 1.41–8.39)] to be significantly associated with IAH. The contents and amounts of fluid infusion were not significantly associated with IAH. There were also significant duration–response effects between duration of glucocorticoid use and IAH; however, pulse glucocorticoid administration was not associated with IAH.ConclusionIn this nested case–control study, we demonstrated a significant association between IAH and high-dose glucocorticoid with significant duration–response effects. Serum sodium concentrations should be monitored carefully in critically ill patients administered prolonged high-dose glucocorticoid.Electronic supplementary materialThe online version of this article (10.1007/s10157-020-01967-9) contains supplementary material, which is available to authorized users.

ICU-Acquired Hypernatremia Is Associated with Persistent Inflammation, Immunosuppression and Catabolism Syndrome.

Developing hypernatremia while on intensive care unit (ICU) is a common problem with various undesirable effects. A link to persistent inflammation, immunosuppression and catabolism syndrome (PICS) can be established in two ways. On the one hand, hypernatremia can lead to inflammation and catabolism via hyperosmolar cell stress, and on the other, profound catabolism can lead to hypernatremia via urea-induced osmotic diuresis. In this retrospective single-center study, we examined 115 patients with prolonged ICU stays (≥14 days) and sufficient renal function. Depending on their serum sodium concentrations between ICU day 7 and 21, allocation to a hypernatremic (high) and a nonhypernatremic group (low) took place. Distinct signs of PICS were detectable within the complete cohort. Thirty-three of them (28.7%) suffered from ICU-acquired hypernatremia, which was associated with explicitly higher signs of inflammation and ongoing catabolism as well as a prolonged ICU length of stay. Catabolism was discriminated better by the urea generation rate and the urea-to-creatinine ratio than by serum albumin concentration. An assignable cause for hypernatremia was the urea-induced osmotic diuresis. When dealing with ICU patients requiring prolonged treatment, hypernatremia should at least trigger thoughts on PICS as a contributing factor. In this regard, the urea-to-creatinine ratio is an easily accessible biomarker for catabolism.

Intensive care unit-acquired hyponatremia in critically ill medical patients

BackgroundPrevious research has focused on intensive care unit (ICU)-acquired hypernatremia; however, ICU-acquired hyponatremia has frequently been overlooked and has rarely been studied in surgical or mixed ICUs. The aim of this study is to investigate the incidence of ICU-acquired hyponatremia, the risk factors associated with its development, and its impact on outcomes in critically ill medical patients.MethodsWe conducted a retrospective cohort study based on the prospective registry of all critically ill patients admitted to the medical ICU from January 2015 to December 2018. Baseline characteristics and management variables were compared between ICU-acquired hyponatremia and normonatremia patients.ResultsOf 1342 patients with initial normonatremia, ICU-acquired hyponatremia developed in 217 (16.2%) patients and ICU-acquired hypernatremia developed in 117 (8.7%) patients. The Sequential Organ Failure Assessment (8.0 vs 7.0, P = 0.009) and Simplified Acute Physiology Score 3 scores (55.0 vs 51.0, P = 0.005) were higher in ICU-acquired hyponatremia patients compared with normonatremia patients. Baseline sodium (137.0 mmol/L vs 139.0 mmol/L, P < 0.001), potassium (4.2 mmol/L vs 4.0 mmol/L, P = 0.001), and creatinine (0.98 mg/dL vs 0.88 mg/dL, P = 0.034) levels were different between the two groups. Net volume balance over first 3 days was higher in ICU-acquired hyponatremia patients (19.4 mL/kg vs 11.5 mL/kg, P = 0.004) and was associated with the development of ICU-acquired hyponatremia (adjusted odds ratio, 1.004; 95% confidence interval, 1.002–1.007; P = 0.001). ICU mortality was similar in both groups (15.2% vs. 14.4%, P = 0.751), but renal replacement therapy was more commonly required in ICU-acquired hyponatremia patients (13.4% vs 7.4%, P = 0.007).ConclusionsICU-acquired hyponatremia is not uncommon in critically ill medical patients. Increased volume balance is associated with its development. ICU-acquired hyponatremia is related to increased use of renal replacement therapy but not to mortality.

Prognostic value of ICU-acquired hypernatremia in patients with neurological dysfunction.

Many studies have indicated that hypernatremia is associated with increased mortality. In this study, we aimed to explore the relationship between intensive care unit (ICU)-acquired hypernatremia and the prognosis of critically neurological patients.Based on serum sodium level in the ICU, 450 patients were divided into 3 groups: 222 had normal serum sodium, 142 had mild hypernatremia, and 86 had severe hypernatremia. Kaplan–Meier and multivariable binary logistic regression analyses were performed to evaluate the prognostic value of hypernatremia in critically neurological patients. Receiver operating characteristic (ROC) curve was constructed for serum sodium levels to determine their roles in predicting ICU mortality.Hypernatremia was significantly related with age, Glasgow Coma Scale (GCS) score, serum sodium, APACHE II score, and serum creatinine. Moreover, the different treatment outcome including mechanical ventilation, the days of stayed in ICU, and Glasgow Outcome Scale score had correlation with serum sodium levels. Old ages, GCS score, therapeutic intervention scoring system (TISS) score, APACHE II score, serum sodium peak, and so on were all associated with the mortality. In addition, hypernatremia was an independent prognostic factor for critically neurological patients by logistic regression analysis (odds ratio = 1.192, 95% confidence interval = 1.135–1.252, P = 0.000). Moreover, we got the sensitivity of 79.4% and specificity of 74.5% in the ROC analysis between peak serum sodium and the mortality. The area under the ROC curve was 0.844, and the optimal cutoff value was 147.55.Our results showed that ICU-acquired hypernatremia may be a potential prognosis marker for critically neurological patients.

Long-term changes in dysnatremia incidence in the ICU: a shift from hyponatremia to hypernatremia.

BackgroundDysnatremia is associated with adverse outcome in critically ill patients. Changes in patients or treatment strategies may have affected the incidence of dysnatremia over time. We investigated long-term changes in the incidence of dysnatremia and analyzed its association with mortality.MethodsOver a 21-year period (1992–2012), all serum sodium measurements were analyzed retrospectively in two university hospital ICUs, up to day 28 of ICU admission for the presence of dysnatremia. The study period was divided into five periods. All serum sodium measurements were collected from the electronic databases of both ICUs. Serum sodium was measured at the clinical chemistry departments using standard methods. All sodium measurements were categorized in the following categories: <120, 120–124, 125–129, 130–134, 135–139, 140–145, 146–150, 151–155, 156–160, >160 mmol/L. Mortality was determined at 90 days after ICU admission.ResultsIn 80,571 ICU patients, 913,272 serum sodium measurements were analyzed. A striking shift in the pattern of ICU-acquired dysnatremias was observed: The incidence of hyponatremia almost halved (47–25 %, p < 0.001), whereas the incidence of hypernatremia nearly doubled (13–24 %, p < 0.001). Most hypernatremias developed after ICU admission, and the incidence of severe hypernatremia (sodium > 155 mmol/L) increased dramatically over the years. On ICU day 10 this incidence was 0.7 % in the 1992–1996 period, compared to 6.3 % in the 2009–2012 period (p < 0.001). More severe dysnatremia was associated with significantly higher mortality throughout the 21-year study period (p < 0.001).ConclusionsIn two large Dutch cohorts, we observed a marked shift in the incidence of dysnatremia from hyponatremia to hypernatremia over two decades. As hypernatremia was mostly ICU acquired, this strongly suggests changes in treatment as underlying causes. This shift may be related to the increased use of sodium-containing infusions, diuretics, and hydrocortisone. As ICU-acquired hypernatremia is largely iatrogenic, it should be—to an important extent—preventable, and its incidence may be considered as an indicator of quality of care. Strategies to prevent hypernatremia deserve more emphasis; therefore, we recommend that further study should be focused on interventions to prevent the occurrence of dysnatremias during ICU stay.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-016-0124-x) contains supplementary material, which is available to authorized users.

Intensive care unit–acquired hypernatremia is an independent predictor of increased mortality and length of stay

PurposeThe purpose of this study is to examine the impact of hypernatremia acquired after intensive care unit (ICU) admission on mortality and length of stay (LOS). Materials and MethodsData for this observational study were collected from patients admitted between January 1, 2008, and September 30, 2010 to 344 ICUs in the eICU Research Institute. ResultsOf the 207702 eligible patients, 8896 (4.3%) developed hypernatremia (serum Na >149 mEq/L). Hospital mortality was 32% for patients with hypernatremia and 11% for patients without hypernatremia (P < .0001). Intensive care unit LOS was 13.7 ± 9.7 days for patients with hypernatremia and 5.1 ± 4.6 for patients without hypernatremia (P < .0001). Multivariate analysis showed that hypernatremia was an independent risk factor for hospital mortality with a relative risk (RR) of 1.40 (95% confidence interval, 1.34-1.45) and ICU LOS with a rate ratio (RtR) of 1.28 (1.26-1.30). The RR for mortality and RtR for ICU LOS increased with increasing severity strata of hypernatremia, but the duration of hypernatremia was not associated with mortality. ConclusionsHypernatremia developed following ICU admission in 4.3% of patients. Hypernatremia was independently associated with a 40% increase in risk for hospital mortality and a 28% increase in ICU LOS. Severity, but not duration of ICU-acquired hypernatremia was associated with hospital mortality.

Anesthesia Literature Review

Anesthesia Literature Review

Intensive care-acquired hypernatremia after major cardiothoracic surgery is associated with increased mortality

Hypernatremia is common in the medical Intensive Care Unit (ICU) and has been described as an independent risk factor for mortality. Hypernatremia has not yet been studied in a collection of ICU patients after cardiothoracic surgery. Therefore, we wanted to determine the incidence of hypernatremia in a surgical ICU and its association with outcomes of critically ill surgical patients. In this retrospective cohort study performed at a surgical ICU of a university hospital in Vienna, patients were admitted to the ICU after major cardiothoracic surgery between May 1999 and October 2007. Data on serum sodium in the ICU, ICU mortality, hospital mortality, and length of ICU stay were collected prospectively. 2,699 patients underwent surgery during the study period, and 2,314 patients were included in the study. Two hundred twenty-one (10%) patients acquired hypernatremia during their ICU stay. Median onset of hypernatremia was on day 4 (2-7). Patients with ICU-acquired hypernatremia had a higher ICU mortality (19%) compared to patients without hypernatremia (8%; p < 0.01). Length of ICU stay was increased in patients with hypernatremia (17 vs. 3 days; p < 0.01). In a multivariate Cox regression, ICU-acquired hypernatremia was an independent risk factor for ICU mortality within 28 days. Hypernatremia is a common event early in the course of critical illness after major cardiothoracic surgery and is independently associated with ICU mortality within 28 days. Future research should focus on the impact of hypernatremia on physiological functions as well as adequate and safe treatment of the electrolyte disorder.

Characterization of intensive care unit acquired hyponatremia and hypernatremia following cardiac surgery

Although intensive care unit (ICU) acquired sodium disturbances are common in critically ill patients, few studies have examined sodium disturbances in patients following cardiac surgery. The objective of this study was to describe the epidemiology of ICU-acquired hyponatremia and hypernatremia in patients following cardiac surgery. We identified 6,727 adults (> or =18 yr) who were admitted consecutively to a regional cardiovascular intensive care unit (CVICU) from January 1, 2000 to December 31, 2006 and were documented as having normal serum sodium levels (133 to 145 mmol.L(-1)) during the first day of ICU admission. ICU-acquired hyponatremia and hypernatremia were defined as a change in serum sodium concentration to <133 mmol.L(-1) or >145 mmol.L(-1), respectively, following ICU day one. A first episode of ICU-acquired hyponatremia and hypernatremia developed in 785 (12%) and 242 (4%) patients, respectively, (95% confidence interval [CI] 11-12% and 95% CI 3-4%, respectively), with a respective incidence density of 4.2 and 1.3 patients per 100 days of ICU admission (95% CI 4.0-4.5 and 95% CI 1.2-1.5). The incidence of ICU-acquired sodium disturbances varied according to the patients' demographic and clinical variables for both hyponatremia (age, diabetes, Acute Physiology and Chronic Health Evaluation [APACHE II] score, mechanical ventilation, length of ICU stay, serum glucose level, and serum potassium level) and hypernatremia (APACHE II score, mechanical ventilation, length of hospital stay prior to ICU admission, length of ICU stay, serum glucose level, and serum potassium level). Compared with patients with normal serum sodium levels, hospital mortality was increased in patients with ICU-acquired hyponatremia (1.6% vs 10%, respectively; P < 0.001) and ICU-acquired hypernatremia (1.6% vs 14%, respectively; P < 0.001). ICU-acquired hyponatremia and hypernatremia are common complications in critically ill patients following cardiac surgery. They are associated with patient demographic and clinical characteristics and an increased risk of hospital mortality.

Tonicity Balance in Patients With Hypernatremia Acquired in the Intensive Care Unit

Hypernatremia is a serious electrolyte disturbance and an independent risk factor for mortality in critically ill patients. In many cases, hypernatremia is an iatrogenic problem that develops in the intensive care unit (ICU). Case series. 45 patients were studied in a medical ICU. For inclusion in the study, patients needed to show an increase in serum sodium concentration to greater than 149 mEq/L from an initial concentration of less than 146 mEq/L. Solute balance, fluid balance, and both. Causes of hypernatremia. The daily mass balance of sodium, potassium, and water over 1- to 3-day intervals was measured while serum sodium levels were increasing. During the study period, 69 of 981 patients (7%) acquired hypernatremia after admission to the ICU. Of these, 45 had sufficient data for evaluation. Maximum serum sodium levels were 150 to 164 mEq/L. The average duration of hypernatremia was 2 days (range, 1 to 10 days), with an average onset on day 5.9 +/- 4.3 of the ICU stay. Patients were classified as having a positive solute balance (n = 17; 38%), negative fluid balance (n = 20; 44%), or both (n = 8; 18%). The most important extrarenal factors contributing to hypernatremia were fever (45%) and diarrhea (18%). Polyuria was observed in 38% of patients and 35% had acute renal failure. Hypertonic solutions were administered to 27% of patients. Retrospective analysis; lack of daily measurement of body weight. ICU-acquired hypernatremia is associated with multiple factors associated with negative fluid and positive solute balance.