Changes In Serum Sodium Concentration Research Articles

Association of baseline serum sodium with long-term outcomes in newly diagnosed coronary heart disease patients without heart failure: a prospective cohort study

Sodium is crucial for maintaining cardiovascular health, especially in relation to heart failure. The impact of baseline serum sodium concentrations on the outcomes of newly diagnosed coronary heart disease (CHD) without heart failure remains unclear. This prospective cohort study included 681 patients who were newly diagnosed with CHD. Cox proportional hazards models and restricted cubic spline (RCS) analysis were used to assess the relationship between serum sodium concentrations and major adverse cardiovascular events. The improvement in traditional prediction models by the addition of serum sodium concentrations was assessed using changes in the C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). During a median follow-up of 51.04 months (IQR: 40.88–53.80 months), 131 events were recorded. Multivariate Cox proportional hazards models showed that the L2 group (136–138.9 mmol/L) had the highest MACE risk. Compared to L2, the hazard ratios (HRs) and 95% confidence intervals (CIs) for the L1 (130–135.9 mmol/L), L3 (139–140.9 mmol/L), L4 (141–142.9 mmol/L), and L5 (143–147.0 mmol/L) groups were 0.31 (0.14–0.70, P = 0.005), 0.48 (030–0.78, P = 0.003), 0.56 (0.34–0.92, P = 0.022), and 0.37 (0.22–0.64, P < 0.001), respectively. Including serum sodium concentrations in the prediction model significantly improved the C-statistic from 0.647 to 0.679 (P = 0.022), with an NRI of 0.338 (P < 0.001) and an IDI of 0.026 (P < 0.001). RCS analysis showed a nonlinear relationship: within the 130–138 mmol/L sodium range, MACE risk gradually increased with higher sodium levels (HR 1.39, 95% CI 1.09–1.76, P = 0.008); whereas within the 138–147 mmol/L range, the risk gradually decreased (HR 0.88, 95% CI 0.80–0.98, P = 0.014). Baseline serum sodium concentrations are significantly associated with long-term cardiovascular risk in newly diagnosed CHD patients, showing an inverted U-shaped relationship, whereas low serum sodium may be specifically linked to higher risks of death and nonfatal myocardial infarction. Further research is needed to explore the impact of long-term changes in serum sodium concentrations on disease prognosis.

The Relationship between Serum Sodium Concentration and Albuminuria: A Retrospective Cohort Study.

Lowering dietary salt intake reduces albuminuria, an early marker of renal damage and a sensitive predictor of adverse cardiovascular outcomes. The mechanisms underlying this effect are uncertain but small changes in serum sodium concentration may be important: this retrospective cohort study investigated the hypothesis that higher serum sodium concentration is a risk factor for albuminuria (defined as a urine albumin:creatinine ratio [UACR], ≥3 mg/mmol). Primary care data from the Royal College of General Practitioners Research and Surveillance Centre were used to identify 47,294 individuals with a UACR result available between April 2010 and March 2015, and no known albuminuria prior to this. Exclusion criteria were missing or abnormal serum sodium concentration at baseline (&lt;135 or &gt;146 mmol/L); age &lt;18 years; diabetes mellitus; decompensated liver disease; heart failure; and stage 5 chronic kidney disease. After adjustment for known risk factors, there was a significant "U-shaped" relationship between serum sodium concentration and albuminuria. The lowest risk was associated with a serum sodium of 138-140 mmol/L. In comparison, the risk of albuminuria was 18% higher with a serum sodium of 135-137 mmol/L and 19% higher with a serum sodium of 144-146 mmol/L. There was no association between serum sodium concentration and blood pressure. The finding of a positive association between higher serum sodium concentration and albuminuria is in support of the hypothesis, but the inverse relationship between serum sodium concentration and albuminuria at lower concentrations warrants further explanation.

Changes in serum sodium concentration during hemodialysis is a predictor of mortality and cardio-cerebrovascular event

Background Previous study consistently showed that lower serum sodium (SNa) was associated with a greater risk of mortality in hemodialysis (HD) patients. However, few studies have focused on the change in SNa (ΔSNa = post-HD SNa – pre-HD SNa) during an HD session. Methods In a retrospective cohort of maintenance HD adults, all-cause mortality and cardio-cerebrovascular event (CCVE) were followed up for a medium of 82 months. Baseline pre-HD SNa and ΔSNa were collected; time-averaged pre-HD SNa and ΔSNa were computed as the mean values within 1-year, 2-year and 3-year intervals after enrollment. Cox proportional hazards models were used to evaluate the relationships of pre-HD and ΔSNa with outcomes. Results Time-averaged pre-HD SNa were associated with all-cause mortality (2-year pre-HD SNa: HR [95% CI] 0.86 [0.74–0.99], p = 0.042) and CCVE (3-year pre-HD SNa: HR [95% CI] 0.83 [0.72–0.96], p = 0.012) with full adjustment. Time-averaged ΔSNa also demonstrated an association with all-cause mortality (3-year ΔSNa: HR [95% CI] 1.26 [1.03–1.55], p = 0.026) as well as with CCVE (3-year ΔSNa: HR [95% CI] 1.51 [1.21–1.88], p = <0.001) when fully adjusted. Baseline pre-HD SNa and ΔSNa didn’t exhibit association with both outcomes. Conclusions Lower time-averaged pre-HD SNa and higher time-averaged ΔSNa were associated with a greater risk of all-cause mortality and CCVE in HD patients.

Dysnatremia

Changes in serum sodium concentrations are frequently encountered by anesthesiologists, are complex and are often inadequately treated. Feared consequences include neurological complications, such as cerebral hemorrhage, cerebral edema and coma. Dysnatremia is always accompanied disturbances in the water balance. Accordingly, these are routinely classified based on the tonicity; however, in the daily routine and especially in the acute setting, the volume status and extracellular volume are often difficult to assess. Severe symptomatic hyponatremia with impending cerebral edema is treated by administration of hypertonic saline solution. If the rise in serum sodium is too rapid, there is arisk of central pontine myelinolysis. In asecond step, the cause of the hyponatremia can be investigated and the appropriate treatment can be initiated. In the case of hypernatremia, the etiology of the disorder must be clarified before treatment. The goal is to compensate for the water deficiency by correcting the cause, specific volume therapy and, if necessary, drug support. Aslow and controlled compensation must be closely monitored in order to avoid neurological complications. An algorithm has been developed that provides an overview of the dysnatremias, aids with making the diagnosis and gives recommendations for treatment measures in the clinical routine.

Hypertonic Saline Infusion for Hyponatremia: Limitations of the Adrogué-Madias and Other Formulas.

Hypertonic saline infusion is used to correct hyponatremia with severe symptoms. The selection of the volume of infused hypertonic saline ( VInf ) should address prevention of overcorrection or undercorrection. Several formulas computing this VInf have been proposed. The limitations common to these formulas consist of (1) failure to include potential determinants of change in serum sodium concentration ([ Na ]) including exchanges between osmotically active and inactive sodium compartments, changes in hydrogen binding of body water to hydrophilic compounds, and genetic influences and (2) inaccurate estimates of baseline body water entered in any formula and of gains or losses of water, sodium, and potassium during treatment entered in formulas that account for such gains or losses. In addition, computing VInf from the Adrogué-Madias formula by a calculation assuming a linear relation between VInf and increase in [ Na ] is a source of errors because the relation between these two variables was proven to be curvilinear. However, these errors were shown to be negligible by a comparison of estimates of VInf by the Adrogué-Madias formula and by a formula using the same determinants of the change in [ Na ] and the curvilinear relation between this change and VInf . Regardless of the method used to correct hyponatremia, monitoring [ Na ] and changes in external balances of water, sodium, and potassium during treatment remain imperative.

Diabetes Insipidus after Vasopressin Withdrawal: A Scoping Review.

The objective of this study is to synthesize the current literature about the relationship between the occurrence of diabetes insipidus (DI), its diagnosis criteria, and management after withdrawal of vasopressin (VP) in critically ill. This scoping review followed the recommendations of Preferred Reporting Items for Systematic Review and Meta-Analyses for Scoping Review (PRISMA-ScR). The search literature was conducted in MEDLINE and EMBASE databases, until March 2022. A manual search was also conducted in order to include articles that were not identified in the initial search performed in the databases. The selection of studies and extraction of data were carried out in a paired and independent manner. There was no restriction regarding the language of publication of the included manuscripts. The analysis included 17 studies (16 case reports and one retrospective cohort). All studies used VP, with a median time of drug infusion of 48 hours (IQR: 16-72) and DI incidence of 1.53%. The diagnosis of DI was based on diuresis output and concomitant hypernatremia or changes in serum sodium concentration, with median time to symptoms onset after discontinuation of VP of 5 hours (IQR: 3-10). The treatment of DI consisted mainly of fluid management and the use of desmopressin. DI after VP withdrawal was present in 51 patients described in 17 studies, but diagnosis and management varied among each report. Using the available data, we propose a diagnosis suggestion and a flowchart for managing patients with DI after withdrawal of VP in the Intensive Care Unit. Multicentric collaborative research is urgently needed to obtain more quality data on this topic. Pérsico RS, Viana MV, Viana LV. Diabetes Insipidus after Vasopressin Withdrawal: A Scoping Review. Indian J Crit Care Med 2022;26(7):846-852.

Changes in Factors Regulating Serum Sodium Homeostasis During Two Ultra-Endurance Mountain Races of Different Distances: 69km vs. 121km.

Overdrinking and non-osmotic arginine vasopressin release are the main risk factors for exercise-associated hyponatremia (EAH) in ultra-marathon events. However, particularly during ultra-marathon running in mountainous regions, eccentric exercise and hypoxia, which have been shown to modulate inflammation, hormones regulating fluid homeostasis (hypoxia), and oxidative stress, could contribute to serum sodium changes in a dose-dependent manner. To the best of our knowledge, the contribution of these factors, the extent of which depends on the duration and geographical location of the race, has not been well studied. Twelve male participants (11 finishers) of the short (69km, 4,260m elevation-gain) and 15 male participants (seven finishers) of the long (121km, 7,554m elevation-gain) single-stage Südtirol Ultra Sky-Race took part in this observational field study. Venous blood was drawn immediately before and after the race. Analyses included serum sodium concentration, copeptin (a stable marker for vasopressin), markers of inflammation, muscle damage and oxidative stress. Heart rate was measured during the race and race time was obtained from the race office. During the short and the long competition two and one finishers, respectively showed serum sodium concentrations >145mmol/L. During the long competition, one athlete showed serum sodium concentrations <135mmol/L. Only during the short competition percent changes in serum sodium concentrations of the finishers were related to percent changes in body mass (r=−0.812, p=0.002), total time (r=−0.608, p=0.047) and training impulse (TRIMP) (r=−0.653, p=0.030). Data show a curvilinear (quadratic) relationship between percent changes in serum sodium concentration and body mass with race time when including all runners (short, long, finishers and non-finishers). The observed prevalence of hypo- and hypernatremia is comparable to literature reports, as is the relationship between serum sodium changes and race time, race intensity and body mass changes of the finishers of the short race. The curvilinear relationship indicates that there might be a turning point of changes in serum sodium and body mass changes after a race time of approximately 20h. Since the turning point is represented mainly by non-finishers, regardless of race duration slight decrease in body mass and a slight increase in serum sodium concentration should be targeted to complete the race. Drinking to the dictate of thirst seems an adequate approach to achieve this goal.

Pre-dialysis Hyponatremia and Change in Serum Sodium Concentration During a Dialysis Session Are Significant Predictors of Mortality in Patients Undergoing Hemodialysis

BackgroundPrevious studies have shown that hyponatremia is associated with greater mortality in hemodialysis (HD) patients. However, there have been few reports regarding the importance of the change in serum sodium (SNa) concentration (ΔSNa) during dialysis sessions. To investigate the relationships of pre-dialysis hyponatremia and ΔSNa during a dialysis session with mortality, we analyzed data from a national registry of Japanese patients with end-stage kidney disease.MethodsWe identified 178,114 patients in the database who were undergoing HD 3 times weekly. The study outcome was 2-year all-cause mortality, and the baseline SNa concentrations were categorized into quintiles. We evaluated the relationships of SNa concentration and ΔSNa with mortality using Cox proportional hazards models.ResultsDuring a 2-year follow-up period, 25,928 patients died. Each 1-mEq/l reduction in pre-HD SNa concentration was associated with a cumulatively greater risk of all-cause mortality (hazard ratio [HR], 1.05; 95% confidence interval [CI], 1.05–1.06). In contrast, a larger ΔSNa was associated with higher all-cause mortality (HR for a 1-mEq/l increase in ΔSNa, 1.02; 95% CI 1.01–1.02). The combination of low pre-HD SNa concentration and large ΔSNa was also associated with higher mortality (HR 1.09; 95% CI 1.05–1.13). Participants with the lowest SNa concentration (≤136 mEq/L) and the highest ΔSNa (>4 mEq/L) showed higher mortality than those with an intermediate pre-HD SNa concentration (137–140 mEq/L) and the lowest ΔSNa (≤2 mEq/L).ConclusionsLower pre-HD SNa concentration and higher ΔSNa are associated with a greater risk of mortality in patients undergoing HD.

Focal Neurological Deficit Secondary to Severe Hyponatraemia Mimicking Stroke.

Hyponatraemia is a common electrolyte abnormality seen by internists. Clinical features of hyponatraemia are primarily related to CNS dysfunction, and depend on the severity and acuity of changes in serum sodium concentration. Neurological manifestations of hyponatraemia range from nausea and malaise, with a mild reduction in the serum sodium, to lethargy, decreased level of consciousness, headache, seizures and coma in extreme cases. Focal neurological deficits are very rare in the setting of hyponatraemia. Here, we describe a patient with acute severe symptomatic hyponatraemia presenting with focal neurological deficits that resolved after correction of acute hyponatraemia.LEARNING POINTSA rare presentation of hyponatraemia is described.Neuroimaging should be performed in patients with focal neurological deficits and hyponatraemia in order to rule out other serious neurological diseases.Correction of severe hyponatraemia can result in resolution of focal neurological deficits.

誤嚥性肺炎後に生じた鉱質コルチコイド反応性低ナトリウム血症の1例(Mineralocorticoid–responsive hyponatremia of the elderly secondary to aspiration pneumonia: a case report)

要旨 67歳の男性。路上で倒れているところを発見され救急要請された。救急隊接触時はJCS I–3R，頚動脈触知可，脈拍 45/分，冷感が強く体温測定不可能であった。当院搬送時はGCS E4V2M5，血圧 69/45mmHg，脈拍53/分，膀胱温は27.1℃，血清Naは109mEq/Lであった。偶発性低体温症，低Na血症による意識障害で救命救急センターに入院となった。補正による血清Naの改善に伴い意識レベルも徐々に改善を認めた。しかし誤嚥性肺炎を合併したため人工呼吸管理が必要であった。人工呼吸管理中より再度低Na血症が進行した。経口，経静脈的にNaの補正を行ったが改善せず，第22病日には121mEq/Lまで低下した。低浸透圧血症，高浸透圧尿症，ADH高値，エコーにて体液過剰が否定的であることから鉱質コルチコイド反応性低Na血症と診断した。輸液負荷，塩分補充に対する反応に乏しかったことから鉱質コルチコイドの補充を追加した。ADHを経時的に測定し正常化したのを確認後に鉱質コルチコイドを漸減し，第78病日に中止した。その後は血清Na値の低下を来すことなく，リハビリ目的に転院した。高齢者はストレスに対する予備力が低下しているため電解質異常を合併しやすい。高齢者の低Na血症の診断において治療が異なるためSIADHとの鑑別が重要である。また血清Na正常化後も鉱質コルチコイドの長期投与が必要である。

Serum sodium concentration and the progression of established chronic kidney disease

BackgroundHigher serum sodium concentration has been reported to be a risk factor for the development of incident chronic kidney disease (CKD), but its relationship with the progression of established CKD has not been investigated. We hypothesised that increased serum sodium concentration is a risk factor for estimated glomerular filtration rate (eGFR) decline in CKD.MethodsThis was a retrospective cohort study using data collected over a 6-year period, with baseline data obtained during the first 2 years. We included patients known to our renal service who had had a minimum of three blood tests every 2 years and an eGFR of < 60 mL/min/1.73 m2 at baseline. Exclusion criteria were renal replacement therapy, diabetes mellitus, heart failure and decompensated liver disease. A multiple linear regression model investigated the relationship between baseline serum sodium and eGFR decline after adjustment for confounding factors.Results7418 blood results from 326 patients were included. There was no relationship between serum sodium concentration and estimated glomerular filtration rate at baseline. After multivariable adjustment, a 1 mmol/L increase in baseline serum sodium was associated with a 1.5 mL/min/1.73 m2 decline in eGFR during the study period (95% CI 0.9, 2.0). A reduction in eGFR was not associated with significant changes in serum sodium concentration over 6 years.ConclusionHigher serum sodium concentration is associated with the progression of CKD, independently of other established risk factors. Conversely, significant alterations in serum sodium concentration do not occur with declining kidney function.

Correction of Hyponatremia May Be a Treatment Stratification Biomarker: A Two-Stage Systematic Review and Meta-Analysis.

Changes in serum sodium concentration ([Na+]serum) can permit evaluation of the treatment effect of vasopressin antagonists (vaptans) in patients with worsening heart failure (HF) or cirrhotic ascites; that is, they may act as a treatment stratification biomarker. A two-stage systematic review and meta-analysis were carried out and contextualized by experts in fluid resuscitation and translational pharmacology (registration ID in the International Prospective Register of Systematic Reviews (PROSPERO): CRD42017051440). Meta-analysis of aggregated dichotomous outcomes was performed. Pooled estimates for correction of hyponatremia (normalization or an increase in [Na+]serum of at least 3–5 mEq/L) under treatment with vaptans (Stage 1) and for clinical outcomes in both worsening HF (rehospitalization and/or death) and cirrhotic ascites (ascites worsening) when correction of hyponatremia is achieved (Stage 2) were calculated. The body of evidence was assessed. Correction of hyponatremia was achieved under vaptans (odds ratio (OR)/95% confidence interval (95% CI)/I2/number of studies (n): 7.48/4.95–11.30/58%/15). Clinical outcomes in both worsening HF and cirrhotic ascites improved when correction of hyponatremia was achieved (OR/95% CI/I2/n: 0.51/0.26–0.99/52%/3). Despite the appropriateness of the study design, however, there are too few trials to consider that correction of hyponatremia is a treatment stratification biomarker. Patients with worsening HF or with cirrhotic ascites needing treatment with vaptans, have better clinical outcomes when correction of hyponatremia is achieved. However, the evidence base needs to be enlarged to propose formally correction of hyponatremia as a new treatment stratification biomarker. Markers for use with drugs are needed to improve outcomes related to the use of medicines.

Histidine-Tryptophan-Ketoglutarate Solution versus Blood Cardioplegia in Cardiac Surgery: A Propensity-Score Matched Analysis.

Choosing a cardioplegic solution is a significant issue in modern cardiac surgery. Although different options are available, the optimal strategy for myocardial protection has not been established. The aim of this study was to compare intraoperative and postoperative effects of histidine-tryptophan-ketoglutarate (HTK) solution with those of standard blood cardioplegia with St Thomas No 2 solution. The study was conducted using a large cohort of adult patients undergoing complex cardiac surgery. This study was a single center retrospective review of prospectively collected data. Between January 2008 and December 2015, 4480 patients underwent cardiac surgery using cardiopulmonary bypass (CPB) and cardioplegic arrest. Patients were divided into a blood cardioplegia group (n = 3852) and an HTK solution group (n = 628). Propensity score matching was used to adjust for differences between the two groups, and 292 matched pairs were identified. The primary end point was Intensive Care Unit (ICU) length of stay (LOS). Secondary end points included intraoperative changes in serum sodium concentration, readmission to ICU, transfusion of blood products, 30-day hospital readmission, 30-day mortality, and the incidence of major postoperative complications.Results: No significant differences were found between the matched groups with regard to baseline characteristics. Aortic cross-clamp and CPB times were longer for the blood cardioplegia (147.4 versus 132.8 min; P < .001). Administration of HTK solution was associated with acute and transient hyponatremia (141 versus 130 mmol/L; P < .001). ICU LOS was comparable between the groups (5.4 versus 5.4 days; P = .585). No significant differences were noted in any other secondary end point. During complex cardiac surgery, both cardioplegia techniques were equivalent in terms of early clinical outcomes.

Rapidity of Correction of Hyponatremia Due to Syndrome of Inappropriate Secretion of Antidiuretic Hormone Following Tolvaptan

Tolvaptan effectively corrects hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but undesired overcorrection can occur. We hypothesized that pretherapy parameters can predict the rapidity of response to tolvaptan in SIADH. Multicenter historical cohort study. Adults with SIADH or congestive heart failure (CHF) treated with tolvaptan for a serum sodium concentration≤ 130 mEq/L at 5 US hospitals. Demographic and laboratory parameters. Rate of change in serum sodium concentration. Spearman correlations, analysis of variance, and multivariable linear mixed-effects models. 28 patients with SIADH and 39 patients with CHF treated with tolvaptan (mean baseline serum sodium, 120.6 and 122.4 mEq/L, respectively) were studied. Correction of serum sodium concentration > 12 mEq/L/d occurred in 25% of patients with SIADH compared to 3% of those with CHF (P<0.001). Among patients with SIADH, the increase in serum sodium over 24hours was correlated with baseline serum sodium concentration (r=-0.78; P<0.001), serum urea nitrogen concentration (SUN; r=-0.76; P<0.001), and estimated glomerular filtration rate (r=0.58; P=0.01). Baseline serum sodium and SUN concentrations were identified as independent predictors of change in serum sodium concentration in multivariable analyses. When patients were grouped into 4 categories according to baseline serum sodium and SUN median values, those with both low baseline serum sodium (≤121 mEq/L) and low baseline SUN concentrations (≤10mg/dL) exhibited a significantly greater rate of increase in serum sodium concentration (mean 24-hour increase of 15.4 mEq/L) than the other 3 categories (P<0.05). Among patients with CHF, only baseline SUN concentration was identified as an independent predictor of change in serum sodium concentration over time. Lack of uniformity in serial serum sodium concentration determinations and documentation of water intake. Baseline serum sodium and SUN values are predictive of the rapidity of hyponatremia correction following tolvaptan use in SIADH. We advise caution when dosing tolvaptan in patients with both low serum sodium and SUN concentrations.

Benefits of Intraoperative Continuous Renal Replacement Therapy During Liver Transplantation in Patients With Renal Dysfunction

BackgroundComparative outcomes of continuous renal replacement therapy during liver transplantation have not been investigated. We retrospectively compared the outcomes of intraoperative continuous renal replacement therapy with those of non-dialytic conservative treatment in patients with pretransplant renal dysfunction. MethodsWe analyzed 240 transplantation patients with preoperative renal dysfunction (estimated glomerular filtration rate <60 mL/min/1.73 m2). ResultsCompared with the non-dialytic conservative treatment group (n = 98), the intraoperative continuous renal replacement therapy group (n = 142) experienced more severe critical illness (as indicated by Model for End-Stage Liver Disease score) and more severe preoperative renal dysfunction, as well as more frequent hepatic encephalopathy, ventilatory care, and intensive care unit admission (P < .005). There were also worse outcomes regarding patient survival, graft survival, recovery of renal function, and postoperative complications. However, the intraoperative continuous renal replacement therapy group significantly escaped volume overload (adjusted odds ratio, 0.396; 95% confidence interval, 0.223–0.703; P = .002) and unnecessary changes in serum sodium concentration ≥10 mmol/L during surgery (adjusted odds ratio, 0.208; 95% confidence interval, 0.065–0.665; P = .008). ConclusionsConsidering the more severe critical illness of the intraoperative continuous renal replacement therapy group but the low frequency of volume overload and serum sodium fluctuation, intraoperative continuous renal replacement therapy could be useful during liver transplantation in critically ill patients with renal dysfunction. Randomized, controlled studies that could demonstrate outcome benefits and indications of intraoperative continuous renal replacement therapy during liver transplantation are needed.

EXERCISE ASSOCIATED HYPONATREMIA (EAH) AND FLUID INTAKE DURING THE 2016 LONDON MARATHON

BackgroundExercise-Associated Hyponatremia (EAH) is a potentially fatal condition during endurance exercise (Petzold et al, 2007). Excessive fluid intake over and above normal fluid losses is the most common risk factor...

Baseline Renal Function Predicts Hyponatremia in Liver Cirrhosis Patients Treated with Terlipressin for Variceal Bleeding.

Objectives Terlipressin is safely used for acute variceal bleeding. However, side effects, such as hyponatremia, although very rare, can occur. We investigated the development of hyponatremia in cirrhotic patients who had acute variceal bleeding treated with terlipressin and the identification of the risk factors associated with the development of hyponatremia. Design and Methods This retrospective, case-control study investigated 88 cirrhotic patients who developed hyponatremia and 176 controls that did not develop hyponatremia and were matched in terms of age and gender during the same period following terlipressin administration. Results The overall change in serum sodium concentration and the mean lowest serum sodium concentration were 3.44 ± 9.55 and 132.44 ± 8.78 mEq/L during treatment, respectively. Multivariate analysis revealed that baseline serum sodium was an independent positive predictor, and the presence of baseline serum creatinine, HBV, DM, creatinine, and shock on admission was independent negative predictors of hyponatremia (P < 0.05). Conclusion The presence of HBV, DM, the baseline serum sodium, shock on admission, and especially baseline creatinine may be predictive of the development of hyponatremia after terlipressin treatment. Therefore, physicians conduct vigilant monitoring associated with severe hyponatremia when cirrhotic patients with preserved renal function are treated with terlipressin for variceal bleeding.

Formulas for fixing serum sodium: curb your enthusiasm.

A variety of formulas have been proposed to predict changes in serum sodium concentration. All are based on an experiment done over 50 years ago by Edelman, who derived a formula relating the plasma sodium concentration to isotopically measured body sodium, potassium, and water. Some of these formulas fail because they do not include urinary losses of electrolytes and water. Even those that include these essential variables are not accurate enough for clinical use because it is impractical to adjust calculations to rapid changes in urinary composition, and because the formulas do not account for changes in serum sodium caused by internal exchanges between soluble and bound sodium stores or shifts of water into or out of cells resulting from changes in intracellular organic osmolytes. Nephrologists should curb their enthusiasm for predictive formulas and rely instead on frequent measurements of the serum sodium when correcting hyponatremia and hypernatremia.

Hypernatremia - Diagnostics and therapy

Hypernatremia is a common electrolyte disorder that reflects an imbalance in the water balance of the body, often resulting from an increased loss of free water compared to sodium excretion. It is rarely based on excessive sodium intake. The clinical presentation is often characterized by a central nervous system dysfunction (confusion, coma) and pronounced thirst (in awake patients). In addition to medical history, the volume status of the patient and the osmolality of urine are leading in the differential diagnosis. Usually, the treatment of hypernatremia - in addition to addressing the underlying cause - is replacing the (absolute or relative) loss of free water by hypotonic infusions, or in case of diabetes insipidus, by application of Desmopressin (Minirin). As rapid changes in serum sodium concentration may have deleterious consequences (osmotic demyelinsiation syndrome), preexisting hypernatremia (>48h) should not be reduced by more than 8-10 mmol/l/day. Close laboratory controls are important. For acute hypernatremia (< 24 hours), hemodialysis is an effective option to rapidly normalize the serum sodium levels. To avoid a rapid drop in sodium concentration that must also be considered when starting a renal replacement therapy in patients with chronic hypernatremia.

Hypertonicity: Pathophysiologic Concept and Experimental Studies.

Disturbances in tonicity (effective osmolarity) are the major clinical disorders affecting cell volume. Cell shrinking secondary to hypertonicity causes severe clinical manifestations and even death. Quantitative management of hypertonic disorders is based on formulas computing the volume of hypotonic fluids required to correct a given level of hypertonicity. These formulas have limitations. The major limitation of the predictive formulas is that they represent closed system calculations and have been tested in anuric animals. Consequently, the formulas do not account for ongoing fluid losses during development or treatment of the hypertonic disorders. In addition, early comparisons of serum osmolality changes predicted by these formulas and observed in animals infused with hypertonic solutions clearly demonstrated that hypertonicity creates new intracellular solutes causing rises in serum osmolality higher than those predicted by the formulas. The mechanisms and types of intracellular solutes generated by hypertonicity and the effects of the solutes have been studied extensively in recent times. The solutes accumulated intracellularly in hypertonic states have potentially major adverse effects on the outcomes of treatment of these states. When hypertonicity was produced by the infusion of hypertonic sodium chloride solutions, the predicted and observed changes in serum sodium concentration were equal. This finding justifies the use of the predictive formulas in the management of hypernatremic states.