Pseudohyponatremia: Mechanism, Diagnosis, Clinical Associations and Management.

Pseudohyponatremia remains a problem for clinical laboratories. In this study, we analyzed the mechanisms, diagnosis, clinical consequences, and conditions associated with pseudohyponatremia, and future developments for its elimination. The two methods involved assess the serum sodium concentration ([Na]S) using sodium ion-specific electrodes: (a) a direct ion-specific electrode (ISE), and (b) an indirect ISE. A direct ISE does not require dilution of a sample prior to its measurement, whereas an indirect ISE needs pre-measurement sample dilution. [Na]S measurements using an indirect ISE are influenced by abnormal concentrations of serum proteins or lipids. Pseudohyponatremia occurs when the [Na]S is measured with an indirect ISE and the serum solid content concentrations are elevated, resulting in reciprocal depressions in serum water and [Na]S values. Pseudonormonatremia or pseudohypernatremia are encountered in hypoproteinemic patients who have a decreased plasma solids content. Three mechanisms are responsible for pseudohyponatremia: (a) a reduction in the [Na]S due to lower serum water and sodium concentrations, the electrolyte exclusion effect; (b) an increase in the measured sample's water concentration post-dilution to a greater extent when compared to normal serum, lowering the [Na] in this sample; (c) when serum hyperviscosity reduces serum delivery to the device that apportions serum and diluent. Patients with pseudohyponatremia and a normal [Na]S do not develop water movement across cell membranes and clinical manifestations of hypotonic hyponatremia. Pseudohyponatremia does not require treatment to address the [Na]S, making any inadvertent correction treatment potentially detrimental.

Psychotropic drug-induced hyponatremia: results from a drug surveillance program-an update.

Hyponatremia (HN) is the most common electrolyte imbalance (defined as a serum sodium concentration Na(S) of  < 130 mmol/l) and often induced by drugs including psychotropic drugs. AMSP (Arzneimittelsicherheit in der Psychiatrie) is a multicenter drug surveillance program that assesses severe or unusual adverse drug reactions (ADRs) occurring during treatment with psychotropic drugs. This study presents data from 462,661 psychiatric inpatients treated in participating hospitals between 1993 and 2016 and serves as an update of a previous contribution by Letmaier et al. (JAMA 15(6):739-748, 2012). A total of 210 cases of HN were observed affecting 0.05% of patients. 57.1% of cases presented symptomatically; 19.0% presented with severe symptoms (e.g., seizures, vomiting). HN occurred after a median of 7 days following the first dose or dose increase. Incidence of HN was highest among the two antiepileptic drugs oxcarbazepine (1.661% of patients treated) and carbamazepine (0.169%), followed by selective serotonin-norepinephrine reuptake inhibitors (SSNRIs, 0.088%) and selective serotonin reuptake inhibitors (0.071%). Antipsychotic drugs, tricyclic antidepressants, and mirtazapine exhibited a significantly lower incidence of HN. The risk of HN was 16-42 times higher among patients concomitantly treated with other potentially HN-inducing drugs such as diuretic drugs, angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, and proton pump inhibitors. Female SSNRI-users aged  ≥ 65 years concomitantly using other HN-inducing drugs were the population subgroup with the highest risk of developing HN. The identification of high-risk drug combinations and vulnerable patient subgroups represents a significant step in the improvement of drug safety and facilitates the implementation of precautionary measures.

Efficacy and safety of tolvaptan after pediatric congenital heart disease surgery.

It is not clear whether tolvaptan is safe and effective irrespective of various underlying clinical conditions including the functional ventricle morphology, chromosomal abnormalities, and renal function after complex pediatric congenital heart disease surgery. Also, the appropriate dose of tolvaptan in these patients has not been previously identified. We retrospectively assessed the urine volume, body weight, patient clinical characteristics, laboratory data, and vital signs before and on days 1 and 7 of the tolvaptan administration after congenital heart disease surgery. Also, we assessed the relationship between the tolvaptan dose and its effects. A total of 86 patients were included the study. The mean time from the surgery to the tolvaptan administration was 23.5 ± 3.7 days. After administering tolvaptan, the urine volume significantly increased and body weight significantly decreased from baseline by days 1 and 7 (p < 0.0001). The urine volume significantly increased more in the survivors than the deceased. Of the 22 patients who had low serum sodium concentrations at baseline, 20 had an increased serum sodium concentration on day 7. The clinical effect of tolvaptan was not affected by the functional ventricle morphology, chromosomal abnormalities, or renal function. There was a positive correlation between the tolvaptan dose and change in the urine volume until a tolvaptan dose of up to 0.3 mg/kg/day but not at more than 0.3 mg/kg/day. Tolvaptan administration is safe and effective after congenital heart disease surgery irrespective of various underlying clinical conditions. Though the urine volume tends to increase until a tolvaptan dose of up to 0.3 mg/kg/day in pediatric congenital heart disease patients, there was no further benefit with more than 0.3 mg/kg/day.

Efficacy of Furosemide, Oral Sodium Chloride, and Fluid Restriction for Treatment of Syndrome of Inappropriate Antidiuresis (SIAD): An Open-label Randomized Controlled Study (The EFFUSE-FLUID Trial).

RATIONALE & OBJECTIVE: First-line therapy for syndrome of inappropriate antidiuresis (SIAD) is fluid restriction. Additional treatment for patients who do not respond to fluid restriction are water restriction with furosemide or water restriction with furosemide and salt supplementation. However, the efficacy of these treatments has never been tested in a randomized controlled study. The objective of this study was to investigate whether, combined with fluid restriction, furosemide with or without sodium chloride (NaCl) supplementation was more effective than fluid restriction alone in the treatment of hyponatremia in SIAD. STUDY DESIGN: Open-label randomized controlled study. SETTING & PARTICIPANTS: Patients with serum sodium concentrations ([Na+]) ≤ 130mmol/L due to SIAD. INTERVENTION(S): Random assignment to 1 of 3 groups: fluid restriction alone (FR), fluid restriction and furosemide (FR+FM), or fluid restriction, furosemide, and NaCl (FR+FM+NaCl). Strictness of fluid restriction (<1,000 or<500mL/d) was guided by the urine to serum electrolyte ratio. Furosemide dosage was 20 to 40mg/d. NaCl supplements were 3g/d. All treatments were continued for 28 days. OUTCOMES: The primary outcome was change in [Na+] at days 4, 7, 14, and 28 after randomization. RESULTS: 92 patients were recruited (FR, n=31; FR+FM, n=30; FR+FM+NaCl, n=31). Baseline [Na+] was 125±4mmol/L, and there were no significant differences between groups. Mean [Na+] on day 4 in all treatment groups was significantly increased from baseline by 5mmol/L (P<0.001); however, the change in [Na+] was not significantly different across groups (P=0.7). There was no significant difference in percentage of patients or time to reach [Na+] ≥ 130 or≥135mmol/L across the 3 groups. Acute kidney injury and hypokalemia (potassium≤3.0mmol/L) were more common in patients receiving furosemide. LIMITATIONS: Open-label treatment. CONCLUSIONS: In patients with SIAD, furosemide with NaCl supplement in combination with fluid restriction did not show benefits in correction of [Na+] compared with treatment with fluid restriction alone. Incidences of acute kidney injury and hypokalemia were increased in patients receiving furosemide. FUNDING: None. TRIAL REGISTRATION: Registered at the Thai Clinical Trial Registry with study number TCTR20170629004.

Factors affecting blood glucose and serum sodium level with intraoperative infusion of 1% dextrose in ringer's lactate in neonates undergoing surgery.

CONTEXT: Under anesthesia, blood glucose level in term neonates varies widely due to stress induced glucose mobilisation due to various factors. Postoperative hyponatremia occurs with intraoperative infusion of large volume of hypotonic fluid. There is a growing consensus on the intraoperative use of 1-4% glucose containing isotonic fluid in them. AIMS: To know the relation of duration of surgery, infusion rate, fluid bolus, blood transfusion with blood glucose level and effect on serum sodium level with intraoperative 1% dextrose ringer's lactate (1% DRL) in neonates undergoing surgery. SETTINGS AND DESIGN: Prospective single-center study in tertiary institute. SUBJECTS AND METHODS: A total of 100 neonates undergoing various surgeries under general anesthesia with or without caudal anaesthesia were included. 1% DRL was used as maintenance and replacement fluid intraoperatively. Blood glucose level at hourly interval throughout surgery and serum sodium concentration before and after infusion was documented. STATISTICAL ANALYSIS USED: Student's t test (two tailed, independent) has been used for statistical analysis. RESULTS: After the infusion of 1% DRL during surgery, mean blood sugar levels were increased above the base line in all neonates at successive hourly interval. Serum sodium levels remained within physiological range in all neonates. CONCLUSION: Intraoperative hyperglycemia is more obvious with higher intravenous fluid infusion rate, prolonged duration of surgery, and requirement of fluid bolus as well as blood transfusion intraoperatively. Use of 1% DRL in neonates undergoing surgery is effective in preventing dysnatremia.

A quantitative approach to intravenous fluid therapy in the syndrome of inappropriate antidiuretic hormone secretion.

BACKGROUND: A wide range of interesting mathematical models has been derived to predict the effect of intravenous fluid therapy on the serum sodium concentration (most notably the Adrogué-Madias equation), but unfortunately, these models cannot be applied to patients with disorders characterized by aberrant antidiuretic hormone (ADH) release, such as the syndrome of inappropriate ADH secretion (SIADH). The use of intravenous fluids in these patients should prompt caution, as the inability of the kidneys to properly dilute the urine can easily result in deterioration of hyponatremia. METHODS: In this report, a transparent and clinically applicable equation is derived that can be used to calculate the estimated effect of different types and volumes of crystalloid infusate on the serum sodium concentration in SIADH patients. As a "proof of concept", we discuss five SIADH patient cases from our clinic. Alternatively, our mathematical model can be used to determine the infusate volume that is required to produce a certain desired change in the serum sodium concentration in SIADH patients. CONCLUSION: The presented model facilitates rational intravenous fluid therapy in SIADH patients, and provides a valuable addition to existing prediction models.

Ad libitum water consumption prevents exercise-associated hyponatremia and protects against dehydration in soldiers performing a 40-km route-march.

BACKGROUND: It remains unclear if ad libitum water drinking, as a hydration strategy, prevents exercise-associated hyponatremia (EAH) during prolonged exercise. The aim of this study was to determine the incidence of EAH within the broader context of fluid regulation among soldiers performing a 40-km route-march ingesting water ad libitum. METHODS: Twenty-eight healthy male soldiers participated in this observational trial. Pre- and post-exercise body mass, blood and urine samples were collected. Blood samples were assessed for serum sodium ([Na+]), glucose, creatinine, urea nitrogen (BUN), plasma osmolality, creatine kinase (CK), and plasma arginine vasopressin (AVP) concentrations. Plasma volume (PV) was calculated using hematocrit and hemoglobin. Urine samples were analyzed for osmolality and [Na+]. Water intake was assessed by weighing bottles before, during and after the march. The mean relative humidity was 55.7% (21.9-94.3%) and the mean dry bulb temperature was 27.1 °C (19.5 °C - 37.0 °C) during the exercise. RESULTS: Twenty-five soldiers (72 ± 10 kg) (Mean ± SD) completed the march in 09:11 ± 00:43 (hr:min). Participants consumed 736 ± 259 ml/h of water and lost 2.8 ± 0.9 kg (4.0% ± 1.4%, P < 0.05) of body mass. Significant (pre-march vs. post-march; P < 0.05) decreases in serum [Na+] (141 mmol/L vs. 136 mmol/L), plasma osmolality (303 mOsmol/kg H2O vs. 298 mOsmol/kg H2O), and serum creatinine (111 µmol/L vs. 101 µmol/L) and urine [Na+] (168 mmol/L vs. 142 mmol/L), as well as significant increases in plasma AVP (2 pg/ml vs. 11 pg/ml), plasma CK (1423 U/L vs. 3894 U/L) and urine osmolality (1035 mOsmol/kg H2O vs. 1097 mOsmol/kg H2O) were found. The soldier (72 kg) with the lowest post-exercise sodium level completed the march in 08:38. He drank 800 ml/h, lost 2% body mass, and demonstrated (pre-post) increases in plasma osmolality (294-314 mOsmol/kg H2O), BUN (20-30 mg/dl), AVP (2-16 pg/ml) and PV (41%). His urine osmolality decreased from 1114 mOsmol/kg H2O to 1110 mOsmol/kg H2O. No participants finished the route-march with a serum [Na+] indicating hypernatremia (range, 134-143 mmol/L). CONCLUSIONS: Ad libitum drinking resulted in 4% body mass loss with a 2 mmol/L serum [Na+] reduction in conjunction with high urine osmolality (> 1000 mOsmol/kg H2O) and plasma AVP. No single hydration strategy likely prevents EAH, but hypernatremia (cellular dehydration) was not seen despite > 2% body mass losses and high urine osmolality.

Early Relowering of Serum Sodium Concentration Overcomes Disturbances in Consciousness during Hyponatremia Overcorrection and Prevents Osmotic Demyelination Syndrome.

A 79-year-old woman without any cerebral hernia symptoms was hospitalized with hyponatremia. After syndrome of inappropriate antidiuretic hormone induced by drugs was diagnosed and water restriction implemented, the patient became comatose during overcorrection caused by the generation of a large volume of electrolyte-free urine. Once the serum sodium concentration was immediately relowered by the administration of desmopressin and 5% glucose solution, the patient's level of consciousness improved dramatically without osmotic demyelination syndrome (ODS) developing. This outcome suggests that, similar to the findings in rat models, relowering the serum sodium concentration as early as possible to counter a disturbance of consciousness during the overcorrection of hyponatremia prevents ODS.

Osmotic Demyelination Unrelated to Hyponatremia.

Osmotic demyelination unrelated to hyponatremia is rarely reported. We present a case of osmotic demyelination in a patient with hypernatremia in the absence of preceding hyponatremia and review previously reported cases of osmotic demyelination in nonhyponatremic patients. We conclude that a rapid increase in serum sodium concentration and plasma tonicity even in the absence of preceding hyponatremia may surpass the brain's capacity for adaptation to hypertonicity and lead to osmotic demyelination in predisposed individuals. Risk factors for osmotic demyelination in patients with chronic hyponatremia and without hyponatremia are probably similar and are usually associated with states of limited brain osmolyte response, such as alcoholism, liver disease (including those undergoing orthotopic liver transplantation), malnutrition, malignancy, pregnancy/postpartum state, severe illness/sepsis, adrenal insufficiency, and metabolic derangements. Clinicians should be vigilant in identifying individuals who may, even in the absence of hyponatremia, have increased susceptibility to osmotic demyelination and avoid rapid fluctuations in serum sodium concentrations in such patients.

Effect of preoperative serum sodium concentration on the early prognosis of liver transplantation recipients / 国际外科学杂志

Objective To analyze the relationship between preoperative serum sodium concentration and preoperative status of liver transplantation recipients and it's effect on early prognosis. Methods Retrospectively collected the clinical data of 281 patients underwent liver transplantation in First Affiliated Hospital of Zhengzhou University from January 2016 to September 2017. According to the preoperative serum sodium concentration, they were divided into hyponatremia group (< 130 mmol/L) 18 patients, normonatremia group (130-145 mmol/L)232 patients and hypernatremia group(> 145 mmol/L) 31 patients. The SPSS 21.0 statistical software was used to analyze the difference of preoperative MELD score, Child-Pugh score, postoperative survival rate and the incidence of graft dysfunction among three groups. Multivariate comparisons of measurement data were performed using analysis of variance. Pairwise comparisons between groups were performed using the LSD-t test. Chi-square tests were used to compare the count data sets. Results The preoperative MELD score was(19.27 ±7.35) scores, Child-Pugh score was(10.39±2.28) scores, serum creatinine concentration was(95.89 ± 49.40) μmol/L in hyponatremia group, the preoperative MELD score was(12.17土8.79) scores(P=0.001), Child-Pugh score was(8.50±2.68) scores (P =0.004) and serum creatinine was(66.07 ±24.13) μmol/L(P <0.05) in normonatremia group, the difference between two groups were statistically significant. There were no significant difference in the length of postoperative ICU stay and postoperative hospital stay among the three groups, there were no significant difference between the 30th and 90th postoperative survival rates and the incidence of graft dysfunction. Conclusions Hyponatremia is an indicator of poor preoperative status in liver transplantation recipients. Preoperative serum sodium concentration has no significant effect on early prognosis of liver transplantation.

"Beer Potomania" - A Syndrome of Severe Hyponatremia with Unique Pathophysiology: Case Studies and Literature Review.

Beer potomania, a unique syndrome of hyponatremia, was first reported in 1972. It is described as the excessive intake of alcohol, particularly beer, together with poor dietary solute intake that leads to fatigue, dizziness, and muscular weakness. The low solute content of beer, and suppressive effect of alcohol on proteolysis result in reduced solute delivery to the kidney. The presence of inadequate solute in the kidney eventually causes dilutional hyponatremia secondary to reduced clearance of excess fluid from the body. Early detection of hyponatremia due to beer potomania in the hospital is necessary to carefully manage the patient in order to avoid neurological consequences as this syndrome has unique pathophysiology. We are reporting two cases, presenting to the emergency department with severe hyponatremia. After a detailed initial evaluation of the patients and labs for hyponatremia, a diagnosis of beer potomania was established in both cases. Considering the unique pathophysiology of beer potomania syndrome, the patients were closely monitored and treated appropriately to prevent any neurological sequelae.

Hyponatraemia: Epidemiology and aetiology in a tertiary care centre in Pakistan.

OBJECTIVE: To determine the incidence, aetiology and epidemiology of hospitalized patients with hyponatraemia. METHODS: Subjects were identified through hospital information system for two consecutive low sodium values (< 130 mEq/L) and charts were reviewed retrospectively. Possible etiologic factors were identified and co-morbidities documented. Management plans were also noted. RESULTS: Among the hospitalized patients the incidence of hyponatraemia was 6.72%. The mean age was 54.8±14.8 years and there were 50% males. The mean serum sodium at presentation was 122 mEq/L. Most common causes were volume depletion (30.6%) and chronic kidney disease (22.6%). Most of the patients had two or more co morbidities. Hyponatraemia at presentation and improvement or worsening during hospital stay did not affect survival of patients. CONCLUSIONS: Hypervolaemic hyponatraemia was the most common presentation in our study.

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.

Effect of low versus high dialysate sodium concentration on blood pressure and endothelial-derived vasoregulators during hemodialysis: a randomized crossover study.

BACKGROUND: Intradialytic hypertension affects ∼15% of hemodialysis patients and is associated with increased morbidity and mortality. While intradialytic hypertension is associated with increases in endothelin 1 relative to nitric oxide (NO), the cause of these imbalances is unknown. In vitro evidence suggests that altering plasma sodium levels could affect endothelial-derived vasoregulators and blood pressure (BP). Thus, we hypothesized that compared to high dialysate sodium, low dialysate sodium concentration would lower endothelin 1 levels, increase NO release, and reduce BP. STUDY DESIGN: 3-week, 2-arm, randomized, crossover study. SETTING & PARTICIPANTS: 16 patients with intradialytic hypertension. INTERVENTION: Low (5 mEq/L below serum sodium) versus high (5 mEq/L above serum sodium) dialysate sodium concentration. OUTCOMES: Endothelin 1, nitrite (NO2(-)), and BP. MEASUREMENTS: Mixed linear regression was used to compare the effect of dialysate sodium (low vs high) and randomization arm (low-then-high vs high-then-low) on intradialytic changes in endothelin 1, NO2(-), and BP values. RESULTS: The average systolic BP throughout all hemodialysis treatments in a given week was lower with low dialysate sodium concentrations compared with treatments with high dialysate sodium concentrations (parameter estimate, -9.9 [95% CI, -13.3 to -6.4] mm Hg; P < 0.001). The average change in systolic BP during hemodialysis also was significantly lower with low vs high dialysate sodium concentrations (parameter estimate, -6.1 [95% CI, -9.0 to -3.2] mm Hg; P < 0.001). There were no significant differences in intradialytic levels of endothelin 1 or NO2(-) with low vs high dialysate sodium concentrations. LIMITATIONS: Carryover effects limited the power to detect significant changes in endothelial-derived vasoregulators, and future studies will require parallel trial designs. CONCLUSIONS: Low dialysate sodium concentrations significantly decreased systolic BP and ameliorated intradialytic hypertension. Longer studies are needed to determine the long-term effects of low dialysate sodium concentrations on BP and clinical outcomes.

Approach to the treatment of the infant with hyponatremia.

Hyponatremia is an electrolyte abnormality that occurs in infancy due to a variety of inherited and acquired disorders. Infants with hyponatremia can present with neurologic symptoms such as vomiting, weakness, and seizures. Common causes of hyponatremia in the infant population are excess ingestion or administration of hypotonic fluids and excessive gastrointestinal salt loss. Hyponatremia in infancy also can be a sign of less common disorders, such as mineralocorticoid deficiency or resistance, and disregulation of arginine vasopressin with impaired free-water removal. Treatment of infants with hyponatremia is dependent on the severity of symptoms and the cause of hyponatremia. In nephrogenic syndrome of inappropriate antidiuresis (NSIAD), fluid retention is due to a gain-of-function mutation in the arginine vasopressin receptor 2 (AVPR2) gene leading to low arginine vasopressin levels. We describe the case of an infant with hyponatremia due to NSIAD, whose mother also has a known mutation in the AVPR2 gene. We report the approach to the treatment of hyponatremia and its unique challenges in infancy.

[Hypernatremia in head-injured patients: friend or foe?]. / Hypernatrémie chez le patient cérébrolésé: utile ou dangereux?

Hypernatremia is defined by a serum sodium concentration of more than 145 mmol/L and reflects a disturbance of the regulation between water and sodium. The high incidence of hypernatremia in patients with severe brain injury is due various causes including poor thirst, diabetes insipidus, iatrogenic sodium administration, and primary hyperaldosteronism. Hypernatremia in the intensive care unit is independently associated with increased mortality and complications rates. Because of the rapid brain adaptation to extracellular hypertonicity, sustained hypernatremia exposes the patient to an exacerbation of brain edema during attempt to normalize natremia. Like serum glucose, serum sodium concentration must be tightly monitored in the intensive care unit.

Evaluation of postoperative short·-term survival rate after liver transplantation for benign end-stage hepatopathy by model for end-stage liver disease score and serum sodium concentration and ascites condition / 中华消化外科杂志

Objective To investigate the efficiency of model for end-stage liver disease(MELD)score,serum sodium concentration and aseites condition in the evaluation of short-term survival rate of patients with benign end-stage hepatopathy after liver transplantation.Methods The clinical data of 98 patients with benign end-stage hepatopathy who had undergone liver transplantation in Fuzhou General Hospital from January 1999 to February 2007 were retrospectively analyzed.The relationship between serum sodium concentration.ascites condition and the prognosis of patients with the same MELD score was analyzed.Kaplan-Meier survival curve was drawn.The 1-year survival rate of the patients was analyzed by chi-square test.The mortality of patients with the same MELD score at the end of the third month after operation was analyzed by Fisher's exact test.Results MELD score of aIJ patients was 15-25 or＞25.The postoperatire 3-month mortality rates of patients with serum sodium concentration≥130 mmol/L were 5%and 15%.which were significantly lower than 33%and 55%of those with serum sodium concentration＜1 30 mmol/L.The difference upon 1-year survival rates between them had statistical significance(x2:12.88,P＜0.05).The postoperative 3-month mortality rates of patients without ascites were 5%and 8%.which were lower than 35%and 57%of those with aseites.and the difference upon 1-year survival rates between them had statistical significance(X2=15.26.P＜0.05).Conclusions It is more accurate to evaluate the short-term survival rate after liver transplantation for benign end-stage hepatopathy by combining the MELD score with serum sodium concentration and ascites condition.

Changes of Atrial Natriuretic Peptide in Patients with Subarachnoid Hemorrhage

Hyponatremia following the subarachnoid hemorrhage has been attributed to the syndrome of inappropriate secretion antidiuretic hormone or salt wasting syndrome. Recently discovered atrial natriuretic peptide(ANP) is known to contol sodium and extracellular fluid homeostasis by increasing renal excretion of sodium. To investigate whether the hyponatremia following the subarachnoid hemorrhage(SAH) is due to changes in plasma ANP, plasma ANP, serum sodium concentration and central venous pressure were measured in 10 patients(CSF ANP as well in some patients) with subarachnoid hemorrhage. The results obtained were as follows. 1) Plasma ANP concentration increased during the acute stage of SAH, being recovered to control levels after 8 days of SAH. 2) ANP concentration was significantly higher in plasma than in CSF. 3) No significant correlation was noted between the plasma ANP and CVP or serum sodium concentration. These results suggest that ANP is not involved in the development of hyponatremia during the acute stage of SAH.