Clinical study on the relationship between liver cirrhosis,ascites,and hyponatremia

BACKGROUND Cirrhosis is a common liver disease,and ascites is one of the common clinical conditions.However,the clinical manifestations of ascites combined with hyponatremia as a high-risk condition and its relationship to patient prognosis have not been fully studied.AIM To explore the clinical manifestations,prognostic factors,and relationships of ascites with hyponatremia in patients with cirrhosis to provide better diagnostic and treatment strategies.METHODS In this study,we retrospectively analyzed the clinical data of 150 patients diagnosed with cirrhosis and ascites between 2017 and 2022.Patients were divided into two groups:ascites combined with hyponatremia group and ascites group.We compared the general characteristics,degree of hyponatremia,complications,treatment,and prognosis between the two groups.RESULTS In the study results,patients in the ascites combined with hyponatremia group showed an older average age(58.2±8.9 years),64.4%were male,and had a significantly longer hospitalization time(12.7±5.3 d).Hyponatremia was more severe in this group,with a mean serum sodium concentration of 128.5±4.3 mmol/L,which was significantly different from the ascites group of 137.6±2.1 mmol/L.Patients with ascites and hyponatremia were more likely to develop hepatic encephalopathy(56.2%vs 39.0%),renal impairment(45.2%vs 28.6%)and infection(37.0%vs 23.4%).Regarding treatment,this group more frequently used diuretics(80.8%vs 62.3%)and salt supplements(60.3%vs 38.9%).Multiple logistic regression analysis identified older age[Odds ratio(OR)=1.06,P=0.025]and male gender(OR=1.72,P=0.020)as risk factors for hyponatremia combined with ascites.Overall,patients with ascites and hyponatremia present a clear high-risk status,accompanied by severe complications and poor prognosis.CONCLUSION In patients with cirrhosis,ascites with hyponatremia is a high-risk condition that is often associated with severe complications.

Varicella-Zoster Virus Encephalitis with Hyponatremia in an Immunocompetent Elderly Patient:A Case Report

As a common cause of viral encephalitis,varicella-zoster virus(VZV)may invade the central nervous system of immunosuppressed patients during reactivation.Herein,we report a rare case of an immunocompetent patient with VZV encephalitis who developed severe hyponatremia and was considered to have a suspected primary infection.The patient was diagnosed with the support of second-generation sequencing and had persistent hyponatremia after being cured.Although rare,this case suggests that VZV encephalitis may occur in unexpected patients and present with unusual clinical manifestations,requiring advanced detection methods and clinical expertise for resolution.

Vasopressin-induced hyponatremia in an adult normotensive trauma patient:A case report

BACKGROUND Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland.In addition to maintaining plasma osmolarity,under hypovolemic or hypotensive conditions,it helps maintain plasma volume through renal water reabsorption and increases systemic vascular tone.Its synthetic analogues are widely used in the intensive care unit as a continuous infusion,in addition to hospital floors as an intravenous or intranasal dose.A limited number of cases of hyponatremia in patients with septic or hemorrhagic shock have been reported previously with vasopressin.We report for the first time a normotensive patient who developed vasopressin-induced hyponatremia.CASE SUMMARY A 39-year-old man fell off a forklift and sustained an axial load injury to his cranium.He had no history of previous trauma.Examination was normal except for motor and sensory deficits.The Imagine test showed endplate fracture at C7 and acute traumatic disc at C7 with cortical degeneration.He underwent cervical discectomy and fusion,laminectomy,and posterior instrumented fusion.After intensive care unit admission post-surgery,he developed hyponatremia of 121-124 mEq/L post phenylephrine and vasopressin infusion to maintain blood pressure maintenance.He was evaluated for syndrome of inappropriate secretion of antidiuretic hormone,hypothyroid,adrenal-induced,or diuretic-induced hyponatremia.At the end of extensive evaluation for the underlying cause of hyponatremia,vasopressin was discontinued.He was also put on fluid restriction,given exogenous desmopressin,and a dextrose 5%in water infusion to prevent osmotic demyelination syndrome caused by sodium overcorrection which improved his sodium level to 135 mmol/L.CONCLUSION The presentation of vasopressin-induced hyponatremia is uncommon in normotensive patients,and the most difficult aspect of this condition is determining the underlying cause of hyponatremia.Our case illustrates that,considering the vast differential diagnosis of hyponatremia in hospitalized patients,both hospitalists and intensivists should be aware of this serious complication of vasopressin therapy.

Hyponatremia in cirrhosis:Pathophysiology and management

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension.The development of ascites in patients with cirrhosis is multi-factorial.Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system,sympathetic nervous system and antidiuretic hormone(ADH).The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume resulting in the development of ascites.Although not apparent in the early stages of cirrhosis,the progression of cirrhosis and ascites leads to impairment of the kidneys to eliminate solutefree water.This leads to additional compensatory mechanisms including non-osmotic secretion of ADH,also known as arginine vasopressin,further worsening excess water retention and thereby hyponatremia.Hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis,and is an important prognostic marker both before and after liver transplant.The management of hyponatremia in this setting is a challenge as conventional therapy for hyponatremia including fluid restriction and loop diuretics are frequently inefficacious.In this review,we discuss the pathophysiology and various treatment modalities,including selective vasopressin receptor antagonists,for the management of hyponatremia in patients with cirrhosis.

Hyponatremia in patients with heart failure

The present review analyses the mechanisms relating heart failure and hyponatremia,describes the association of hyponatremia with the progress of disease and morbidity/mortality in heart failure patients and presents treatment options focusing on the role of arginine vasopressin(AVP)-receptor antagonists.Hyponatremia is the most common electrolyte disorder in the clinical setting and in hospitalized patients.Patients with hyponatremia may have neurologic symptoms since low sodium concentration produces brain edema,but the rapid correction of hyponatremia is also associated with major neurologic complications.Patients with heart failure often develop hyponatremia owing to the activation of many neurohormonal systems leading to decrease of sodium levels.A large number of clinical studies have associated hyponatremia with increased morbidity and mortality in patients hospitalized for heart failure or outpatients with chronic heart failure.Treatment options for hyponatremia in heart failure,such as water restriction or the use of hypertonic saline with loop diuretics,have limited efficacy.AVP-receptor antagonists increase sodium levels effectively and their use seems promising in patients with hyponatremia.However,the effects of AVP-receptor antagonists on hard outcomes in patients with heart failure and hyponatremia have not been thoroughly examined.

Case of inappropriate ADH syndrome:Hyponatremia due to polyethylene glycol bowel preparation

Colonoscopic screening has been reported to reduce deaths from colorectal cancer.Adequate bowel preparation is essential for this and safety is an important issue in choosing the methods.Polyethylene glycol(PEG)is regarded as a safe method for cleansing,especially compared with oral sodium phosphate.Here,we present a case of hyponatremia caused by the syndrome of inappropriate antidiuretic hormone(ADH)syndrome after PEG precolonoscopic cleansing resulting in generalized tonic-clonic seizures.A 62-year-old women had ingested PEG for precolonoscopic bowel cleansing.While waiting for the colonoscopy,she developed a stuporous mentality and generalized tonic-clonic seizures,which did not correlate with brain magnetic resonance imaging.Her serum sodium level was 113 mEq per liter and laboratory analyses were consistent with inappropriate ADH syndrome.Her thyroid and adrenal functions were normal.There were no malignancies,infections,respiratory disorders or central nervous disorders and she had no history of taking either diuretics or other medications,which might have caused inappropriate ADH syndrome.She was treated with 3%hypertonic saline and showed a complete neurological recovery as her sodium levels recovered.Follow-up visits showed the patient to have a normal sodium level without neurologic deficits.This case shows that inappropriate ADH syndrome can be caused by PEG preparation,which implies that physicians have to be aware of the possible side effects of this colonic cleansing approach and mindful of the possible ensuing symptoms.

Thiazide-associated hyponatremia in the elderly： what the clinician needs to know

Thiazide-induced hyponatremia is one of the main causes of decreased sodium levels in elderly individuals. This review presents the current evidence regarding the thiazide-associated hyponatremia. Thiazide-associated hyponatremia is observed mainly in patients with certain risk factors such as those receiving large doses of thiazides, having much comorbidity, such as heart failure, liver disease or malignancy, and taking several medications, such as non-steroidal anti-inflammatory drugs, selective serotonin re-uptake inhibitors or tricyclic antide- pressants. Sodium concentration should be monitored in patients with risk factors for developing thiazide-associated hyponatremia and clini- cians should measure promptly serum sodium levels in patients with neurologic signs indicating reduced sodium levels. The clinical and biochemical profile of patients with thiazide-associated hyponatremia may be that of extracellular volume depletion or the syndrome of inap- propriate antidiuretic hormone secretion （SIADH）. The investigation of possible thiazide-associated hyponatremia includes the exclusion of other causes of decreased sodium levels and the identification of the characteristics of hyponatremia due to thiazides （extracellular volume depletion-related or SIADH-like）. Treatment should be carefully monitored to avoid serious neurologic complications due to overcorrection. Clinicians should discourage prescribing thiazides in patients with a history of diuretic-associated hyponatremia and should prefer low doses of thiazides in patients with risk factors for developing thiazide-associated hyponatremia.

Autoimmune polyglandular syndrome type 3 complicated by mineralocorticoid-responsive hyponatremia of the elderly

We experienced the first case with autoimmune polyglandular syndrome type 3(anti-thyroid peroxidase ant ib ody-positive hypothyroidism and anti-glutamic acid decar boxylase antibody-positive diabetes) complicated by miner alocorticoid-responsive hyponatremia of the elderly.This case is also a rare slowly progressive insulin-dependent diabetes mellitus(SPIDDM) case,for which the patient has been treated for many years with sulfonylurea or glinide.Our observation also demonstrated that glucose metabolism in autoimmune diabetes such as SPIDDM is influenced by appetite,thyroid function and glucocorticoid effect.

Extrapontine myelinolysis caused by rapid correction of pituitrin-induced severe hyponatremia: A case report

BACKGROUND Severe hyponatremia is considered a rare complication of pituitrin,which is widely used for the treatment of pulmonary hemorrhage.However,the management of pituitrin-associated hyponatremia can be challenging because a rapid correction of hyponatremia may cause the development of osmotic demyelination syndrome,resulting in life-threatening neurological injuries.CASE SUMMARY A 20-year-old Chinese man with massive hemoptysis developed symptomatic hyponatremia(116 mmol/L)after therapy by a continuous intravenous drip of pituitrin.To normalize his serum sodium,a hypertonic saline infusion was applied for 3 d,and the pituitrin administration was stopped concurrently.Then,an overly rapid increase in serum sodium level(18 mmol/L in 24 h)was detected after treatment.One day later,the patient experienced a sudden onset of generalized tonic-clonic seizures,as well as subsequent dysarthria and dystonia.Magnetic resonance imaging revealed increased signal intensity in the bilateral symmetric basal ganglia on the T2-weighted images,compatible with a diagnosis of extrapontine myelinolysis.The patient received an intravenous administration of high-dose corticosteroids,rehabilitation,and neurotrophic therapy.Finally,his clinical abnormalities were vastly improved,and he was discharged with few residual symptoms.CONCLUSION Physicians should be fully aware that pituitrin can cause profound hyponatremia and its correction must be performed at a controlled rate to prevent the development of osmotic demyelination syndrome.

Hepatic encephalopathy complicated with hyponatremia and acid-base disturbance and its prognosis

Objective:To improve the diagnosis and therapeutic effect of occurrence and development of hyponatremia and disorder of acid-base balance among patients with hepatic encephalopathy(HE) by elucidating the regularity and mechanism,as well as its influence on prognosis.Methods:327 HE patients admitted to our hospital from January 1990 to June 2010 were enrolled.Meanwhile 316 patients hospitalized in the medical department of the same hospital were chosen as the control group.Patients in both groups were given the same methods to measure arterial blood gas parameters(pH value,PaCO2,[HCO3-],TCO2,BE and SaO2),blood biochemistry([Na+],[K+],[Cl-]),liver function,kidney function and blood glucose,serum sodium,and thereupon tocalculate the anion gap(AG) and the potential [HCO3-],and acid-base balance disorder.Results:Among the 327 HE patients,hyponatremia was found in 188 cases(57.4%),of whom 132 patients died(70.2%).While among the 316 patients in control group,68 presented with hyponatremia(21.5%),and 19 died(27.9%).The incidence and mortality were significantly different between the two groups(P<0.001).All the 327 patients presented with different degrees of acid-base balance disorder and 178 died(54.4%),in whom 164(50.2%) belonged to simple acid-base balance disorder and 74(45.1%) died,136(41.6%) were dual acid-base balance disorder and 80(58.8%) died,27(8.2%) were triple acid-base disturbance and 24(88.9%) died.Whereas in the control group only 83 patients(26.2%) were recognized as simple and dual acid-base balance disorder,and 18(21.7%) died.There was higher incidence of acid-base balance disorder and mortality rate in HE group than control one(P<0.001).Conclusion:Hyponatremia is valuable to judge HE patients' prognosis.The key parameters in the judgment and evaluation on acid-base balance disorder among HE patients are the change of pH values and serum electrolyte values.When pH value ≤ 7.30 or > 7.55,it generally suggests a poor prognosis.

Hyponatremia in the acute phase of spinal cord trauma: Review

Hyponatremia is a common electrolyte disturbance usually observed in neurosurgical patients undergoing surgical management of traumatic, as well as, nontraumatic intracranial pathology. The spinal cord trauma is also associated with occasional development of such hyponatremia;it usually occurs within the first two-weeks of the injury. Hyponatremia can lead to alterations of consciousness, convulsions, coma, cardiac arrhythmias and on rare occasions, death. Authors present a practical oriented review of the literature.

The Prevalence of Hyponatremia in Pulmonary Tuberculosis Patients, a Tertiary Care Hospital Experience from Pakistan

Introduction: Tuberculosis (TB) is one of the major public health problems in Pakistan. Our country ranks fifth in tuberculosis high-burden countries worldwide. Hyponatremia is considered as one of the most common and important electrolyte abnormality in Pulmonary TB (PTB) patients. This study will show the prevalence of hyponatremia in PTB in our population. Objective: To evaluate the prevalence of hyponatremia in pulmonary tuberculosis patients. Study Design: Cross-sectional, descriptive study at Jinnah postgraduate medical centre Karachi from August 2017 to August 2018. Material and Methods: In this cross-sectional study, all patients with TB admitted in chest ward were enrolled. Patients having tuberculous meningitis, syndrome of inappropriate Ant diuretic hormone (SIADH), Renal failure, pneumonia, Cirrhosis taking medicines (diuretics, ACEI, and ARBs) were excluded. A pre-designed questionnaire was used to assess hyponatremia and its potential causes other than TB. Chi-square or Fischer exact test was used to identify factors associated with hyponatremia. Results: Ninety-six patients with mean age were 40.14 ± 13.02 years (ranging 18 - 65 years). Predominantly, patients were females 50 (52.08%). Overall Serum Na, Mean ± SD was 130.53 ± 6.99 (Ranging 110 - 146). Sixty one patients (63.5%) were younger than 40 years. Forty patients (41.66%) were smokers: 16 (16.7%) had diabetes mellitus (DM), and 15 (15.6%) had hypertension. Sixty-nine (71.87%) patients had hyponatremia of which 45 (73.77%) were less than 40 years (p = 0.375). Diabetes mellitus, female gender, smoking, hypertension and duration of disease were not associated with increased risk of hyponatremia having P Values: p = 0.082, p = 0.39, p = 0.57, p = 0.20 and p = 0.45 respectively. Conclusion: Hyponatremia is associated with tuberculosis and is more common with diabetes, hypertension, smoking and young age.

Analysis of the incidence and influencing factors of hyponatremia before ^(131)I treatment of differentiated thyroid carcinoma

BACKGROUND Hyponatremia is a common clinical electrolyte disorder.However,the association between hyponatremia and acute hypothyroidism is unclear.Acute hypothyroidism is usually seen in patients who undergo preparation for radioactive iodine therapy.AIM To analyze the incidence and influencing factors of hyponatremia in a condition of iatrogenic acute hypothyroidism in patients with differentiated thyroid cancer(DTC)before ^(131)I treatment.METHODS The study group consisted of 903 DTC patients who received ^(131)I treatment.The clinical data before and after surgery,as well as on the day of ^(131)I treatment were analyzed.According to the blood sodium level before ^(131)I treatment,patients were divided into the non-hyponatremia group and hyponatremia group.Correlations between serum sodium levels before ^(131)I treatment and baseline data were analyzed.Univariate analysis and binary logistic regression were performed to identify the influencing factors of hyponatremia.RESULTS A total of 903 patients with DTC,including 283(31.3%)males and 620(68.7%)females,with an average age of 43.8±12.7 years,were included in this study.The serum sodium levels before surgery and ^(131)I treatment were 141.3±2.3 and 140.5±2.1 mmol/L,respectively(P=0.001).However,the serum sodium levels in males and females before ^(131)I treatment were lower than those before surgery.Patients aged more than 60 years and less than 60 years also showed decreased serum sodium levels before ^(131)I treatment.In addition,the estimated glomerular filtration rate(eGFR)in males and females decreased before ^(131)I treatment compared with those before surgery(P=0.001).Moreover,eGFR in patients over 60 years and under 60 years decreased before ^(131)I treatment,when compared with that before surgery.There were no significant differences in serum potassium,calcium,albumin,hemoglobin,and blood glucose in patients before surgery and ^(131)I treatment(P>0.05).Among the 903 patients,23(2.5%)were diagnosed with hyponatremia before ^(131)I treatment,including 21 cases(91.3%)of mild hyponatremia and 2 cases(8.7%)of moderate hyponatremia.Clinical data showed that patients with mild hyponatremia had no specific clinical manifestations,while moderate hyponatremia cases were mainly characterized by fatigue and dizziness,which were similar to neurological symptoms caused by hypothyroidism and were difficult to distinguish.Correlation analysis showed a correlation between serum sodium before ^(131)I treatment and the preoperative level(r=0.395,P=0.001).There was no significant correlation between blood sodium and thyroid-stimulating hormone(TSH)levels and urine iodine before ^(131)I treatment(r=0.045,P=0.174;r=0.013,P=0.697).Univariate analysis showed that there were significant differences in age,sex,history of diuretic use,distant metastasis,preoperative blood sodium,blood urea nitrogen(BUN),eGFR,TSH and urinary iodine between the two groups(all P<0.05).Logistic regression analysis showed that factors such as history of diuretic use,distant metastases,preoperative sodium and BUN were all influencing factors of hyponatremia.The Hosmer and Lemeshow test(c2=2.841,P=0.944)suggested a high fit of the model.Omnibus tests of model coefficients indicated the overall significance of the model in this fitted model(P<0.05).Preoperative serum sodium was a significant factor associated with pre-^(131)I therapy hyponatremia(OR=0.763;95%CI:0.627-0.928;P=0.007).CONCLUSION The incidence of hyponatremia induced by ^(131)I treatment preparation was not high.Preparation for radioactive iodine therapy was not a risk factor for the development of hyponatremia in thyroid cancer patients.

Severe cyclophosphamide-related hyponatremia in a patient with acute glomerulonephritis

Cyclophosphamide is frequently used to treat cancer,autoimmune and renal diseases,such as rapidly progressive glomerulonephritis.Its side effects are well-known,including bone marrow depression,infections,alopecia,sterility,bladder malignancy and hemorrhagic cystitis.Moreover,in some cases cyclophosphamide use has been related to the onset of hyponatremia,by development of a syndrome of inappropriate antidiuresis.Indeed,severe hyponatremia has been previously reported in patients treated with high-dose or moderate-dose of intravenous cyclophosphamide,while only few cases have been reported in patients treated with low dose.Here,we discuss a case of a syndrome of inappropriate antidiuresis followed to a single low-dose of intravenous cyclophosphamide in a patient with a histological diagnosis of acute glomerulonephritis,presenting as acute kidney injury.After cyclophosphamide administration(500 mg IV),while renal function gradually improved,the patient developed confusion and headache.Laboratory examinations showed serum sodium concentration dropped to 122 mmol per liter associated with an elevated urinary osmolality of 199 mO sm/kg,while common causes of acute hyponatremia were excluded.He was successfully treated with water restriction and hypertonic saline solution infusion with the resolution of the electrolyte disorder.This case,together with the previous ones already reported,highlights that electrolyte profile should be strictly monitored in patients undergoing cyclophosphamide therapy in order to early recognize the potentially lifethreatening complications of acute water retention.

Hyponatremia in the Emergency Department: Could Biomarkers Help in Diagnosis and Treatment?

Objective: Hyponatremia is the most common electrolyte imbalance. The initial treatment decision is based on clinical evaluation of patient volume status but an accurate assessment is difficult, particularly differentiating mild hypovolemia from euvolemia. The aim of this study is to examine if biomarkers are valuable in the early determination of volume status and SIADH diagnosis. Methods: Blood samples were collected from an unselected patient population at entry to the Emergency Department. If the plasma sodium level (P-Na) was ≤125 mmol/L, the sample was frozen for further analysis. Mid-regional pro-atrial natriuretic peptide (MR-proANP), proadrenomedullin (MR-proADM), C-terminal prepro-vasopressin (copeptin), pro-endothelin-1 (proET-1) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were analysed. A comprehensive assessment of volume status and underlying causes was made after discharge blinded for biomarker results. Results: A total of 81 patients were included. A well substa ntiated volemic state (hypo/eu/hypervolemia) was established in 72 patients (mean age 76 years, 65% women, median P-Na 119 mmol/L). A significant association was observed between MR-proANP levels and volemic state (p = 0.0001). Data was specifically analysed with respect to distinguishing hypo- from euvolemia (n = 59) using logistic regression. In a crude analysis, MR-proANP was significantly related to euvolemia (OR: 2.54 per SD of MR-proANP, 95% CI 1.32 - 4.86, p = 0.005) and remained so after the multivariate backward elimination model (OR: 2.45 per SD of MRproANP, 95% CI 1.22 - 4.91, p = 0.012.), whereas the other studied biomarkers were not. Copeptin levels were not associated with a diagnosis of SIADH. Conclusions: MR-proANP may be of value in early determination of volume status in hyponatremic patients.

Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia

Hyponatremia, serum sodium 〈 135 mEq/L, is themost common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the causes of hyponatremia has hampered the delivery of appropriate therapy. This is especially applicable to differentiating syndrome of inappropriate antidiuresis （SIAD） from cerebral salt wasting （CSW） or more appropriately, renal salt wasting （RSW）, because of divergent therapeutic goals, to water-restrict in SIAD and administer salt and water in RSW. Differentiating SIAD from RSW is extremely diffcult because of identical clinical parameters that defne both syndromes and the mindset that CSW occurs rarely. It is thus insuffcient to make the diagnosis of SIAD simply because it meets the defned characteristics. We review the pathophysiology of SIAD and RSW, the evolution of an algorithm that is based on determinations of fractional excretion of urate and distinctive responses to saline infusions to differentiate SIAD from RSW. This algorithm also simplifes the diagnosis of hyponatremic patients due to Addison’s disease, reset osmostat and prerenal states. It is a common perception that we cannot accurately assess the volume status of a patient by clinical criteria. Our algorithm eliminates the need to determine the volume status with the realization that too many factors affect plasma renin, aldosterone, atrial/brain natriuretic peptide or urine sodium concentration to be useful. Reports and increasing recognition of RSW occurring in patients without evidence of cerebral disease should thus elicit the need to consider RSW in a broader group of patients and to question any diagnosis of SIAD. Based on the accumulation of supporting data, we make the clinically important proposal to change CSW to RSW, to eliminate reset osmostat as type C SIAD and stress the need for a new defnition of SIAD.

Prevalence of hyponatremia in acute medical admissions in tropical Asia Pacific Australia

Objective:To determine prevalence of hyponatremia in acute medical admissions in Northern Australasia.Methods:We studied 469 consecutive acute medical admissions to a hospital in Australia's Far North Queensland during the colder months of June and July 2012.Prevalence of hyponatremia and its relationship with gender,age,diagnosis and prognosis in acute medical admissions were investigated.Results:On admission,hyponatremia(plasma sodium<136 mmol/L)was present in 39.4%of patients,with mild(130—135 mmol/L),moderate(126-129 mmol/L)and severe?126 mmol/L)hyponatremia being present in 25.2%,10.7*and 3.6*respectively.Overall,adding together admission hyponatremia with that developing during admission,45.2%of patients were affected with 11.5%moderate hyponatremia cases and 4.1%severe ones.Hypokalemia and hyperkalemia were present in 17.0%and 18.1*,respectively.Overall,275/469 patients(58.6*)presented with an electrolyte abnormality.There were significant correlations of hyponatremia with age but not with gender and in-hospital mortality.Prevalence of hyponatremia was high across all diagnostic categories.Conclusions:The prevalence of hyponatremia appears to be high in the tropical North Australian population,being the highest prevalence reported amongst acute hospital admissions.The previously reported correlations with age and mortality do appear to hold good for this population with a high prevalence of electrolyte disorders.Further prospective analysis on a larger population in the area is needed to confirm our findings.

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 m Osmol/kg H2O vs. 298 m Osmol/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 m Osmol/kg H2O vs. 1097 m Osmol/kg H2O) were found. The soldier(72 kg) with the lowest postexercise sodium level completed the march in 08:38. He drank 800 ml/h, lost 2% body mass, and demonstrated(prepost) increases in plasma osmolality(294–314 m Osmol/kg H2O), BUN(20–30 mg/dl), AVP(2–16 pg/ml) and PV(41%). His urine osmolality decreased from 1114 m Osmol/kg H2O to 1110 m Osmol/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 m Osmol/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.

Desmopression is an effective adjunct treatment for reversing excessive hyponatremia overcorrection

We report a case of a 50-year-old malnourished African American male with hiccups, nausea and vomiting who was brought to the Emergency Department after repeated seizures at home. Laboratory evaluations revealed sodium(Na+) 107 mmol/L, unmeasurably low potassium, chloride < 60 mmol/L, bicarbonate of 38 mmol/L and serum osmolality 217 m Osm/kg. Seizures were controlled with 3% saline Ⅳ. Once nausea was controlled with iv antiemetics, he developed large volume free water diuresis with 6 L of dilute urine in 8 h(urine osmolality 40-60 m Osm/kg) and serum sodium rapidly rose to 126 mmol/L in 12 h. Both intravenous desmopressin and 5% dextrose in water was given to achieve a concentrated urine and to temporarily reverse theacute rise of sodium, respectively. Serum Na+ was gradually re-corrected in 2-3 mmol/L daily increments from 118 mmol/L until 130 mmol/L. Hypokalemia was slowly corrected with resultant auto-correction of metabolic alkalosis. The patient discharged home with no neurologic sequaele on the 11 th hospital day. In euvolemic hyponatremic patient, controlling nausea may contribute to unpredictable free water diuresis. The addition of an antidiuretic hormone analog, such as desmopressin can limit urine output and prevent an unpredictable rise of the serum sodium.

Polydipsia, hyponatremia and rhabdomyolysis in schizophrenia: A case report

The prevalence of polydipsia among patients with schizophrenia is 6%-20%. Around 10%-20% of patients with polydipsia may develop hyponatremia and even complicated with rhabdomyolysis. Here we presented a 40-year-old man with schizophrenia, who had received paliperidone 15 mg/d for more than one year, and polydipsia was noted. In Jan, 2014, he developed hyponatremia(Na 113 m Eq/L) with consciousness disturbance. After 3% Na Cl(500 cc/d) intravenous supplement for three days, the hyponatremia was corrected, but rhabdomyolysis developed with a substantial elevation in the level of creatine kinase(CK) to 30505 U/L. After hydration, the CK level gradually decreased to 212 U/L. Both the hyponatremia itself and quick supplementation of Na Cl can cause rhabdomyolysis. If rhabdomyolysis is not recognized, insufficient hydration or water restriction for polydipsiamay further exacerbate the rhabdomyolysis with a lethal risk. In this case, we highlight the possible complication of rhabdomyolysis with polydipsia-induced hyponatremia. In addition to monitoring the serum sodium level, the monitoring of CK is also important; and switching of antipsychotic may improve the polydipsia.